Category: Alzheimer’s Disease

Abstract

Alzheimer’s Disease is relevant among most of the world’s population today. It is a disease that effects the cognitive function, memory, and language in an individual’s daily life. Now Alzheimer’s Disease has no cure, is untreatable, and the most significant cause is not really known. Also, traditional methods of diagnosing and care are not that efficient. Researchers have been driven to making a connection between the composition of the microbiota inside the gastrointestinal tract and cognitive decline. It is stated that these microorganisms are causing an effect outside of their organ systems, specifically the central nervous system, and by altering the composition it can possibly reduce the neuroinflammatory properties. Another suggestion researchers have put forth is that exercise and probiotic supplementation can have a beneficial impact on cognitive decline. By introducing additional good bacteria into the body as well as maintaining the body system at a healthy state it can prolong the cognitive aging process. Researchers are also attempting to provide the public with better methods and radiotracers for brain imaging to be able to diagnose Alzheimer’s Disease at an earlier stage. If these more advanced protein radiotracers and diagnosis tests can detect the disease earlier than it can be detected now, then it will give physicians a better chance of confronting the disease with the patient. Possible future implications include advancing diagnosis methods and formulating newer medications to delay the neurological aging process. It can even be thought to bring about the studies of looking for an Alzheimer’s Disease cure.

Introduction

Alzheimer’s Disease is a neurodegenerative disease that affects millions of individuals every year. Currently, Alzheimer’s Disease is the most common type of neurodegenerative disease, in comparison to Parkinson’s and Huntington’s Diseases (Alzheimer’s Association, 2018). It is the most common cause of Dementia, the underlying group of symptoms that are exhibited with the disease. Alzheimer’s Disease specifically affects the neurons in the brain. It is when an individual’s brain accumulates a high amount of beta-amyloid proteins and the neurons begin to degenerate or ultimately become destroyed (Alzheimer’s Association, 2018). While age and genetic mutation seem to be the most common risk factors for Alzheimer’s Disease, it may seem to be that women are more susceptible to being diagnosed with it due to their longevity (Alzheimer’s Association, 2018). Professionals seem to think that there might be ways to prevent or even treat Alzheimer’s Disease due to its link to other organ systems in the human body. In addition to the brain’s natural aging process, scientists believe that there is a connection between the body’s gut microbiome and mental capability. Since the gut is home to billions of microorganisms, it is possible they can have a role in the progress of disease outside of the gastrointestinal tract (Abraham et al., 2019). This association can lead to therapeutic methods or even prevention through healthier lifestyle choices. Probiotic supplementation may also prove beneficial due to a leaky gut having influence on inflammatory response and neuromodulatory mechanisms (Leblhuber et al., 2018). Given that the number of individuals effected by this disease is growing exponentially being able to detect it at an early stage of its development can aid in the treatment of its symptoms. Unlike current imaging techniques, diagnosing this disease early with new radiotracers can aid with tracking its progression and evaluate the effectiveness of therapeutic drug options (Harada et al, 2016). In this review, I will be discussing the correlation between nutritional habits, therapeutic methods, and early detection for Alzheimer’s Disease.

Background Info

Alzheimer’s Disease is a degenerative disease that effects the cognitive abilities in individuals. Throughout the progression of this disease the brain goes through the process of decaying. It is possible for outside environmental factors to contribute to this decaying; however, hereditary, age, and genetics are the biggest contributors to contracting this disease (Alzheimer’s Association, 2018). Out of those three risk factors, age has the most impact on determining the development of Alzheimer’s Disease. It seems to be more prevalent in the elderly in comparison to middle-aged adults. Most of the individuals who have been diagnosed with this disease tend to be 65 or older (Alzheimer’s Association, 2018). As the individuals age past that specific threshold, the percentage of neurological degeneration begins to increase even more. An individual’s family history does need to be considered as well. Even though it is not a needed for an individual to develop this disease, it is more likely for someone to be diagnosed with it if they have a first-degree relative with the disease (Alzheimer’s Association, 2018). An individual’s hereditary can play a crucial role in mapping out the genes passed down from parent to offspring. The last major risk factor, genetics, can provide the most obvious sign of Alzheimer’s Disease which is the accumulation of excess cholesterol in the bloodstream and/or proteins in the brain (Alzheimer’s Association, 2018). Specifically, the APOE gene is what provides this symptom. There are three forms of this APOE gene: e2, e3, and e4. Depending on which specific combination the offspring receives from each parent can determine the chances of the offspring contracting Alzheimer’s Disease and at what stage of their life. Inheriting two copies of the APOE-e4 gene increases the risk the most which is 8-12-fold (Alzheimer’s Association, 2018). Unfortunately, these are not the only risk factor that can contribute to Alzheimer’s Disease diagnoses. A wide variety of contributions can make an effect such as: cardiovascular disease, healthy lifestyle choices, cognitive training, or even sex. Studies show that females have a higher chance of contracting Alzheimer’s Disease than men because they tend to live longer (Alzheimer’s Association, 2018).

Symptoms/Diagnosis

Alzheimer’s Disease can make itself known through a variety of signs and symptoms. The most common cause of dementia is Alzheimer’s Disease. The difference between the two is that dementia is a group of symptoms while Alzheimer’s is the underlying disease. Dementia can manifest itself as cognitive and problem-solving issues as well as having difficulty with memory (Alzheimer’s Association, 2018). Most individuals diagnosed with Alzheimer’s Disease have neuropsychiatric symptoms, or NPS. NPS is when the patient exhibits certain behaviors along the lines of apathy, agitation, and psychosis which can have a major effect on daily life (Eikelboom et al., 2019). In the mild, or early stages, of Alzheimer’s Disease individuals can still go about their daily lives independently but might need some help with certain tasks to ensure safety and effectiveness. On the other hand, as the disease progresses during the later stages daily life becomes a struggle. This is when the individual will be needing assistance with activities such as taking a bath, eating, getting dressed, or even using the restroom. In the most severe stages, the patient is bed-bound and can no longer help themselves. This can leave a significant impact on the patient’s physical health since it can increase their chances of getting blood clots, problematic infections, or even have difficulties swallowing food (Alzheimer’s Association, 2018). Overall, diagnosing Alzheimer’s Disease can be quite tedious since there is not one way to do so. Doctors can determine if an individual has dementia; however, it is difficult to find out why (Alzheimer’s Association, 2018). Since there is no single way to diagnose it, doctors perform a serious of tests to come to a conclusive evaluation. Among these tests are: obtaining a medical and family history, asking a family member for evaluations of the patient, cognitive and neurological tests, and blood tests and brain imaging to see for high counts of beta-amyloid (Alzheimer’s Association, 2018). An accumulation of amyloid-B and tau proteins are presymptomatic changes that lead to Alzheimer’s Disease as well as cortical thinning (Preische et al., 2019).

Diet and Nutrition

The well-being of the neurovascular system plays a significant role with cognitive capability. Researchers have shown through their studies that microorganisms located inside the gut can regulate the neurovascular integrity (Ma et al., 2018). Specifically, it was tested on mice if a ketogenic diet, KD, intervention can alter the microorganisms in the GI tract to improve neurovascular functions. After a 16-week trial, it showed that with the assistance of KD there was an increase in function of CBF transports on the blood brain barrier, which helps clear the abundant amounts of amyloid-beta in the brain. This was linked with the increased count of good gut microbiota and diminished the bad pro-inflammatory ones (Ma et al., 2018). Thus, it was proven that a ketogenic diet intervention can heighten neurovascular functions while improving gut microbiota and, in the end, reduce the risk of contracting Alzheimer’s Disease (Ma et al., 2018).

In today’s world population obesity has risen significantly as well as metabolic disorders (Solas et al., 2017). Specifically, cardiovascular and type 2 diabetes have this increase in frequency. Research has shown that there is a specific link between obesity and Alzheimer’s Disease. Even though the reasons behind this are currently unknown, there are some suggestions that it could be due to the gut-brain axis or even the central inflammation process (Solas et al., 2017). Studies have shown that the activation of the inflammatory system in metabolic disease can spread to the brain tissues which in turn causes Alzheimer’s Disease. This specific inflammation can be influenced by changes in the microorganisms in the GI tract (Solas et al., 2017). Research has concluded that unbalanced diets, or even obesity, can have an impact on cognitive dysfunction or age-related disorders (Solas et al., 2017). This ties in with the inflammation happening at the peripheral nervous system. This inflammation then travels into the central nervous system where the brain is located and causes dysfunction of the synapses or begins atrophy of the brain (Solas et al., 2017). It might not be clear what initiates the inflammation at the peripheral level; however, this does give a better understanding of how microorganisms in the GI tract can affect an individual’s neurological state (Solas et al., 2017).

Research has concluded that there seems to be a bidirectional communication between the intestines and the brain, referring to it as the gut-microbiota-brain axis (Lombardi et al., 2018). With studies pointing out how an altered microbiome and neuroinflammatory diseases go hand in hand, it is still unclear in most cases if it is due to one another. It has been pointed out and proven that an individual’s diet contributes to the type of microorganisms in the GI tract and in turn the immune system (Lombardi et al., 2018). Several studies identify changes in these microorganisms in neuroimmune diseases; however, they cannot point out just yet if it causes the disease itself or is a result of it (Lombardi et al., 2018). Theses observations and results can lead to many new methods of approaching a disease in the near future. It can lead to the possibility of altering gut microorganism as a treatment option for neuroimmune and neuroinflammatory diseases (Lombardi et al., 2018).

Studies performed on mice have repeatedly shown how changes in the gut has contributed to deposits of amyloid-beta in the brain; however, it does not say much about how it associates with humans (Vogt et al., 2017). In this study, a fecal test was performed on healthy patients and patients diagnosed with Alzheimer’s Disease. The results of this study showed that in patients diagnosed with Alzheimer’s Disease the microorganisms in the gut have a decreased diversity compared to healthy patients (Vogt et al., 2017). Differences were found in the quantity of a wide range of bacteria. To be specific, there was a decrease in Firmicutes, increase in Bacteroidetes, and decrease in Bifidobacterium in Alzheimer’s patients (Vogt et al., 2017). The findings of this study prove that in addition to other neurodegenerative disease, Alzheimer’s Disease is associated with alterations to the gut microbiota.

Furthermore, another potential determining factor of the gut microbiota composition could be bile acids. It seems that bile acids are altered and deregulated in Alzheimer’s Disease (MahmoudianDehkordi et al., 2018). Bile acids are produced by the liver specifically and metabolized by the gut microorganisms when clearing cholesterol (MahmoudianDehkordi et al., 2018). In this study, bile acid serums were tested from a few groups of participants: healthy individuals, early mild cognitive impairment individuals, late mild cognitive impairment individuals, and Alzheimer’s Disease individuals. Serum ratios were compared to cognition, diagnosis, and genetic variants (MahmoudianDehkordi et al., 2018). Test results showed that in Alzheimer’s patients there was a significant decrease in serum concentration compared to the healthy test participants. The Alzheimer’s Disease patients also showed an increase in bacteria produced in the bile acids. This conclusion confirmed the significant role of the gut-liver-brain axis in the progression of Alzheimer’s Disease (MahmoudianDehkordi et al., 2018).

Therapeutic Methods

At this moment in time Alzheimer’s Disease does not seem to be treatable. There may be way to prolong the aging process; however, there is no definitive way to treat the symptoms. Recently, scientists have suggested that exercise and probiotic supplementation can help slow down the neurodegenerative progress (Abraham et al., 2019). In this study, researchers tested genetically modified mice that carry the Alzheimer’s Disease gene. This were tested on whether exercise training, probiotic supplementation, or a combination of both had better cognitive abilities compared to untreated Alzheimer’s Disease mice (Abraham et al., 2019). After the treatment was completed the different groups of mice were subjected to a series of maze and obstacle tests to determine their cognitive abilities. In the end, the results showed that the group with the combined exercise and probiotic treatments significantly out-performed the other three groups (Abraham et al., 2019). Thus, the combination treatment proved to help decrease the abundant amount of amyloid-beta in the central nervous system and reduce the neuroinflammatory properties (Abraham et al., 2019).

Looking back to the relationship between gut microorganisms and the central nervous system, treatment of those gut bacteria can prove to be beneficial in treating the overall Alzheimer’s Disease. Researchers in this study tested twenty patients with Alzheimer’s Disease before and after a four-week probiotic supplementation schedule. The test included biomarkers of immune activation, gut inflammation markers, and composition of gut microorganisms in fecal specimens (Leblhuber et al., 2018). After the four-week treatment the test concluded that there was a noteworthy decay of fecal zonulin concentrations while there was a growth in Faecalibacterium prausnitzii (Leblhuber et al., 2018). These results illustrate how Alzheimer’s patients that are given a multispecies probiotic supplementation had an increase in diversity of microorganisms in the GI tract. This diverse composition proves beneficial with potential activation of neurological and immunologic processes (Leblhuber et al., 2018). Even though it may sound like all positive results, further studies are recommended by the researchers to figure out consequences of over-supplementation.

Even though there is a lot of correlation with systems outside of the central nervous systems with the brain, there are still some specific factors inside the brain that seem to lead to Alzheimer’s Disease. Meningeal lymphatic vessels inside the brain oversee the draining of macromolecules from the central nervous system (Da Mesquita et al., 2018). Basically, their role is waste removal of abundant proteins. In this study, researchers tested whether impaired meningeal lymphatic vessels had an impact on cognitive function in mice. The test was conducted on three groups of mice and one of the groups was injected with Visudyne with photoconversion, a meningeal lymphatic vessel damaging drug (Da Mesquita et al., 2018). In comparison to the other two controlled groups, the group injected with this specific drug had a significant meningeal lymphatic vessel dysfunction. These mice were no longer able to remove that abundant amount of amyloid-beta from the meninges and caused the cognitive impairment Alzheimer’s Disease promotes. In the end, the results show that this meningeal lymphatic function might be a site for potential therapeutic treatment to prevent or delay the aging process in neurological disease like Alzheimer’s (Da Mesquita et al., 2018).

Even though researchers are searching for methods of treatment through how our body’s organ systems interact with each other, there seems to be a natural occurring product that proves beneficial in the treatment of Alzheimer’s. Bryostatin 1 is an extremely rare marine product that has the potential to eradicate HIV/AIDS, play an intricate part in cancer immunotherapy, and even treat Alzheimer’s Disease (Wender et al., 2017). Since it is such a limited and uncommon natural product, scientists are attempting to synthesize it in clinical studies. This particular study shows that attempts made by scientists to synthesize Bryostatin 1 is revealing a wider range of possible alternate treatment products (Wender et al., 2017). These alternative synthetically accessible products seem to be more effective and better endured by cells in tests (Wender et al., 2017).

Early Detection

With most of the population’s focus centered on treatment methods, another important aspect of disease control is early detection. Early detection of Alzheimer’s Disease can prove crucial by being able to focus on the symptoms as soon as possible. Most cognitive assessments rely on decades old methods which are questionable on their early detection efficacy (Loewenstein et al., 2018). Early detection can prove crucial in prevention before the neurodegeneration spreads throughout the brain. In this study it is shown that controlled learning and assessing the performance of an individual’s memory capacity can be the most effective route in comparison to uncontrolled learning paradigms (Loewenstein et al., 2018). Examples of these memory tests are those that use memory binding, proactive interference, and retroactive interference (Loewenstein et al., 2018). These tests give the opportunity for the individual to be their own standard. Their initial performance is used as the control and is compare with additional trials (Loewenstein et al., 2018).

Brain imaging is a particularly effective step towards diagnosing Alzheimer’s Disease. In order to take a PET image of an individual’s brain a radiotracer is needed to bind to specific parts of the brain as well as contrast at a high intensity. The traditional radiotracer of choice is called F-THK5117. In this study, researchers tested a new novel tau PET tracer called F-THK5351 (Harada et al., 2016). This radiotracer binds to specific tau protein fibrils and proved to have a higher binding rate in these test trials than traditional methods. The Alzheimer’s patients treated in this study not only showed a faster binding rate to proteins but also a significantly higher intensity image of the brain proteins (Harada et al., 2016).

Researchers are improving their methods of early diagnosis of Alzheimer’s Disease, coming up with different ways to easily detect the symptoms. These improved methods of choice are faster than traditional ways to detect and diagnose a patient. In this study, researchers proposed a new method system to classify patients with Alzheimer’s Disease and mild cognitive impairment through 3D magnetic resonance imaging (Zhang et al., 2015). 3D MRI’s were taken and pre-processed for each of the 180 subjects in the test. They were then processed several times again with specific wavelet transforms to extract wavelet coefficients from the image (Zhang et al., 2015). After the processing steps were completed, the images were then analyzed to test the specific accuracy on all the classifiers used to process the images, three individual classifiers and three multiclass methods (Zhang et al., 2015). In the end, the researchers were able to state that WTA-KSVM + PSOTVAC was the best classifier and significantly outperformed the entire experimental group for the best accuracy (Zhang et al., 2015).

Furthermore, in this study researchers planned on testing the detection of Alzheimer’s Disease in its early stages by using magnetic resonance elastography. MRE is noninvasive tool that is used to measure certain characteristics of tissues in vivo (Munder et al., 2018). Researchers in this study used female mice that carried the Alzheimer’s Disease gene and applied the MRE at different stages of the disease early on in its progression. The results showed that by detecting alterations in the diversity, density, and mobility of the cell types in the hippocampus with the MRE, Alzheimer’s Disease can be determined at an early stage (Munder et al., 2018). The MRE being delicate enough to detect these changes is crucial.

In this last study, researchers attempted to make a connection between retinal imaging and diagnosing Alzheimer’s Disease. Retinal imaging for diagnosing can prove to be a noninvasive form of Alzheimer’s detection as well as an earlier specific form (Koronyo et al., 2017). Individuals that exhibit traditional symptoms of Alzheimer’s Disease will also show high amounts of amyloid-B protein inside their retinas. These researchers took a group of normal individuals and compared retina images to those of Alzheimer’s patients. The results showed that in the retinal images, Alzheimer’s patients exhibited retinal amyloid index scores 2.1 times higher (Koronyo et al., 2017). This states that Individuals with Alzheimer’s Disease have an abundant amount of protein deposits inside their retinas. In turn, this study brought to light a more feasible and less invasive way to detect these amyloid-B deposits in patients which can lead to a more practical way to diagnose Alzheimer’s Disease (Koronyo et al., 2017).

Conclusion

Alzheimer’s Disease is the most common neurodegenerative brain disorder that effects millions of individuals worldwide each year. Prevention methods are constantly sought after since Alzheimer’s Disease is still an untreatable disease. In this review, Alzheimer’s Disease was discussed in terms of its link with diet habits, the possibility of new therapeutic methods, and improved forms of early detection. In particular, researchers are identifying the correlation between nutritional habits and the gut microbiota composition causing an effect in cognitive abilities. Researchers are also finding out that probiotic supplementation and a regulated exercise regimen can prove to be a sufficient therapeutic method to reduce the neuroinflammatory process. Finally, these researchers are identifying new radiotracers that have a better ability of binding with amyloid-B proteins in the brain which can lead to a better method of early detection of the underlying disease. With these new findings brought to light it can advance the diagnosis methods used today as well as bring the possibility of delaying the neurological aging process through new medications. We can hope that this can propel new studies into an Alzheimer’s Disease cure somewhere in the near future.

Literature Cited

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Currently scientist and doctors are working together to build a bridge between the potential connection that is associated with microbes and Alzheimer’s disease. At this moment, there is no cure for this irreversible, progressive brain disorder. This disorder slowly destroys the memory’s ability to retain and remember information as well as thinking skills, and eventually as it progresses it affects the ability for patients to carry out simple tasks. However, research is currently being conducted to help us better understand the possible contributions microbes can offer to this degenerative disease.

Introduction

Alzheimer’s disease is one of the leading causes of behavioral and cognitive impairment in today’s society. This progressive disease destroys areas of important mental function such as, memory and thinking skills. Many patients often report their first symptoms around their mid-60s. Alzheimer’s disease is the most common cause of dementia among aging adults. Currently there is no adequate clinical treatment or cure for this disease. However, results gathered from a recent genome-wide associate study indicated that a considerable portion of Alzheimer’s relevant gene signals are in fact not located within the gene coding regions. This suggest that the contribution of the epigenetic or environmental factors to Alzheimer disease are a risk. The potential contribution that is currently being recognized is understanding how pathogenic microbes are associated to both aging and Alzheimer’s disease. With the use of new sequencing and bioinformatic technologies for interrogating the genetics of complex microbial communities and microbial-host interactions we have been able to make great strides in this area of research. Important changes that have been recognized in Alzheimer’s disease include inflammation, immunological aberrations, brain cell atrophy, amyloid genesis, altered gene expression, and cognitive deficits. These symptoms have also been associated as a consequence of microbial infection. In fact, various viruses and other microbes are often present in the brain of elderly people, these microbes while normally dormant can reactivate with stress and immunosuppression. However, scientist and researchers debate on whether or not these microbes are simply opportunistic infections linked with an aging mind. Or whether they are contributing to the progression and decline of the central nervous system that in turn is leading to the development of Alzheimer’s disease. In this paper we will review some of the more recent studies conducted relating microbes and the potential contributions that these pathogens have on neurological dysfunction, while specifically aiming to target Alzheimer’s disease connections.

Discussion

At this point there is one major question we have to answer, and that is, how broad is the range of pathogens that can be linked to Alzheimer’s disease and are they simply opportunist infections of a degenerating brain? Alzheimer’s disease has been associated with a prominent inflammatory component characteristic of infection. There are multiple infectious agents that scientist have proposed to be the etiological cause of Alzheimer’s. Nonetheless, from what I’ve seen there seems to be a connection between microbes and Alzheimer’s disease. However, with the limited amount of definitive studies produced. I can only presume that either Alzheimer’s patients are particularly subjected to fungal infections for an unknown reason. Or conversely, it also seems possible that the infections being produced are the cause of Alzheimer’s disease or at the minimum a contributor to its etiology. At this point in time I don’t think there is enough research or studies being produced to lead us to an absolute answer.

Conclusion

Furthermore, at this point there seems to be no definitive answer on whether or not these microbes are the cause of neurodegeneration that in turn is leading to Alzheimer’s disease. However, there is defiantly a connection with increased microbes located in those who are suffering from Alzheimer’s disease. Hopefully with more research in the coming years we will be able to create a more definitive correspondence and help clarify this possibility.

Memory loss and cognitive decline are common symptoms among people diagnosed with Dementia. Over time, these primary symptoms progress (Alzheimer’s disease) and often lead to inadequate self-care or even the failure to remember family members, especially a significant other. In the opening scene of The Notebook, one of the main characters (Allie) gazes out her window and imagines a young man (Noah) rowing his canoe. It is this scene that begins Allie’s journey of remembering her relationship with Noah. The plot centers around a young man named Noah who works at a lumber yard and falls in love with a young woman named Allie who eventually suffers from Alzheimer’s disease. Throughout the film, Noah spends each day retelling the story of his relationship with Allie by reading from her notebook where she wrote “Read this to me and I’ll come back to you” (The Notebook, 2004). Based on this, Noah believes that this notebook is the only way to spark Allie’s memory of their life together.

Although the film does not explicitly reveal that Allie has Alzheimer’s disease it can be inferred from her disorientation, confusion, memory lapses (both anterograde and retrograde amnesia) and lack of communication when Noah and family members interact with her. Over the course of the film, Allie’s declarative memory becomes worse. She has no recollection of how she met and fell in love with Noah (episodic) nor does she remember Noah’s name or even her children and grandchildren’s names (semantic). An example that illustrates Allie’s inability to recognize her own children and grandchildren (facial agnosia) is when they came to visit her and she said “Nice to meet you” as if she had never met them before. Even though Allie’s declarative memory is severely impaired, her skill memory (nondeclarative) is still intact. She not only can play the piano, but she can read sheet music. Allie’s ability to play the piano is an example of a closed perceptual-motor skill because it involves processing sensory inputs and executing fine motor finger movements. Thus, procedural memories are distinct from declarative memories because they can be retrieved without conscious awareness.

In another scene, Noah and Allie are eating dinner together. After dinner, Noah turns on the radio to hear a song from when they were young that they always danced to. He asks Allie to dance and it is in this moment that she remembers Noah. The song not only triggered her memory of Noah, but it also sparked her remembrance that the story he read to her was about them. Even though Allie does not remember the specific details of her relationship with Noah, she remembers how dancing with Noah made her feel. It is the experience of dancing with Noah when she was young and the emotion she felt in the past that enabled her to remember him in this moment. This relates to mood congruence because Allie was able to recall her memory of Noah since her emotional state while dancing in this moment matched how she felt when this memory of dancing was encoded in the past. Overall, this scene exemplifies the power of emotion and how it influences memory encoding and retrieval because if an experience has intense emotion tied to it, an individual, even Allie with Alzheimer’s disease, is more likely to remember it.

With regards to the neural basis, Alzheimer’s is a degenerative brain disease. This means that Allie’s memory loss is due to the death of neurons and synapses within her cerebral cortex. Since neurons are undergoing apoptosis, her cortex is thinner than a person without Alzheimer’s disease. As the disease progresses and becomes more severe, neuronal death increases so much that the temporal lobe, frontal cortex, hippocampus, cingulate gyrus, and parietal lobe begin to atrophy. More specifically, amyloid plaques and neurofibrillary tangles are the factors that cause this extensive loss of synapses and neurons in the brain. If the protein beta amyloid builds-up in the brain without being broken down, it leads to increased protein deposits (plaques) between neurons, which disrupts cell-to-cell communication. Since plaques prevent cells from communicating with each other; cell death results. The other factor that is thought to contribute to Alzheimer’s disease is neurofibrillary tangles, which are abnormal protein (tau) fibers inside neurons that cluster together. As tau proteins accumulate in the brain, they disrupt neuronal signaling between cells, which eventually causes cells to die. Individuals without Alzheimer’s disease do have some amyloid plaques and neurofibrillary tangles in their brains, but this is normal due to aging. Allie has an abnormal number of amyloid plaques and neurofibrillary tangles in her brain due to Alzheimer’s disease, which is what lead to her neurocognitive decline.

As for my Rotten Tomatoes review of The Notebook, I do not think that Alzheimer’s disease was authentically portrayed through Allie’s character. My rationale for this is because Alzheimer’s disease is more than just memory loss. Alzheimer’s disease includes difficulty completing complex tasks, a degeneration of language (aphasia), an impaired ability to carry out motor activities (apraxia), and personality changes. Allie did not exhibit any of these symptoms besides memory loss. Regarding this, I think Allie was supposed to be depicted in the film as having a late-stage of Alzheimer’s disease, but the way she actually appeared was to be in the early stage of Alzheimer’s disease. My reasoning for this is because I believe that an individual who was in a late-stage of Alzheimer’s would not have such an upkept physical appearance as Allie did, be as active as her, or talk as much as she did. An individual with late-stage Alzheimer’s disease would seldom speak, inadequately care for himself or herself, and possibly be bedridden. Ultimately, The Notebook is not only the most cliché film, but it also inaccurately depicts Alzheimer’s disease which is why it is rated 53% on the Tomatometer.

Reference

1. Harris, L., & Johnson, M. (Producers), Cassavetes, N. (Director). (2004). The Notebook [Motion Picture]. United States: New Line Cinema.

Introduction

Music is the universal language of mankind, allowing communication across cultural and linguistic boundaries. It is expressed and shared by all ages from an unborn child to an elderly person. Every culture around the world has some form of music and song, each with their purpose, some might be to accompany a dance, soothe an infant, express love or express grief or many other purposes. Whilst it has these enormous numbers of benefits, what specifically caught my interest was the link between music and its ability to enhance cognitive functions to help promote healthy aging for older people. It was during a conversation with a close friend of mine, who happens to be a leisure and lifestyle worker at an aged care that, that I truly understood how research from articles such as ‘Lifespan Memory for Popular Songs’ (Bartlett & Snelus, 1980) and others truly impact the leisure activity planning process of these workers. James C Bartlett is a key theorist, whose work has influenced many the researchers in this field to examine and explore the link between music and elderly people with cognitive impairments such as memory loss. Bartlett is known as a pioneer in researching how people perceive and recall non-verbal information, and avantgarde researcher in a large number of fields regarding memory. Additionally to being a researcher who publications has been cited over three-thousands times, his bachelor’s and doctoral psychology degree allowed him to become the head of the doctoral program for cognition and neuroscience in the School of Behavioral and Brain Science at The University of Texas. Bartletts’ article Lifespan Memory for Popular Songs, examined how middle-aged and elderly subjects long term memory performed. His findings implied that certainly popular songs during one’s life were held in long term memory as people aged and that the temporal judgments were based on episodic memory for information at least partially independent of lyric representation. This article although it was one of Bartlett’s earlier works, certainly was one of the findings that initiated the idea of MEAMs, Music Evoked Autobiographical Memory (Janata, Tomic, & Rakowski, 2007). MEAMs’ played a key role in helping those with memory loss impairments, music allowed them to access memories and connect with their young self as well as with their loved ones. This was one of the key ideas that took my attention, as our autobiographical memories are our life stories, this helps us, specifically patients with neurological disorders to gasps a sense of self that they might be lost due to their illness. Another significant research of Bartlett was his work regarding the comparison of recognition of melodies with young, elderly, and elderly Alzheimer patients(Barlett, Halpern, & Dowling, 1995). This opened up doors to other research with Alzheimer patients, as it indicated how these patients were more liberal in recognizing traditional tunes than modern tunes. Similarly, another work of his found that early-stage Alzheimer adults were able to near perfectly discriminate familiar tunes, like holiday tunes(Halpern & Bartlett, 2010).

Article 1 – Characterisation of music-evoked autobiographical memories

Music has always been crucial to many lives, highlighting highs and lows in one’s life. A traditional way of exploring MEAMs has been to explore how music evokes autobiographical memories and emotions associated with them, however, most of these studies focus on the musical pieces themselves such as their title, the singer, or the year it was popular. These methods tended to overlook the memory attributes that served as the focus, Janata and her colleagues explored this component of whether participants were able to describe characteristics of memories evoked by said music and to what extent they were able to connect with the evoked memories (Janata et al., 2007). In their article titled Characterization of music-evoked autobiographical memories, they build on previous studies that compare semantic and episodic knowledge concerning autobiographical knowledge. They do not just build on previous studies but also try to explore the common challenges faced by articles in the field of MEAMs, such as finding a suitable method (Janata et al., 2007). Some previous methods have required participants to report on aspects of memories elicited by cue words or life events (Crovitz & Schiffman, 1974) whilst some attempted a more longitudinal method, allowing initial periods of days during which participants recorded events which were then followed by a test period where the memory recorded early was tested (Cabeza et al., 2004; Levine et al.,2004; Thompson, Skowronski, Larsen, & Betz, 1996; Wagenaar, 1986). Janata and her associated took into account the advantages of these designs and their challenges and decided on a hybrid method to examine MEAMs’, where some questions where presented with a fixed scales and others asking for extra descriptions from participants of their memories. Although the findings of this article weren’t distinctively aimed for the elderly age group, its findings established a normative baseline measure of the frequency for which participants identified songs as autobiographically salient and the degree of detail in which participants described the memories evoked by the music. These findings were quite impactful in the field of MEAMs’ as they provided evidence that musical fragments had potential retrieval cues for autobiographical memories, thus a useful tool for further studies on different levels of autobiographical knowledge. Although the findings were quite meaningful, they weren’t able to pinpoint the exact cause of their results, thus faced some of the same challenges past researchers faced, not being able to distinguish where the reported memories were because they were encoded to a higher extent at the time of emotional salient event or whether the because participants were motivated to describe the memories experienced more intensely at that moment (Janata et al., 2007). The findings did back up some of the interactions I have had with my grandad, 80 years of age, who has always tended to recall certain songs from his youth as well as his tricenarian days to a greater extent, the findings explained how this is probably because of how he has a stronger positive emotional connection to those certain songs.

Article 2- Memory for Melodies and Lyrics in Alzheimer’s disease

Memory for Melodies and Lyrics in Alzheimer’s disease (Cuddy et al., 2012) explanatory research design attempts to explore whether that musical memory is preserved in Alzheimer’s dementia (AD) type patients. This research builds upon their previous study (Cuddy & Duffin, 2005), as one of their aims of the current study was to evaluate the reliability of their previous findings. This was achieved through extending their sample size of Alzheimer participants, their previous study had only one severe AD case, whilst the current had 50 Alzheimer participants who were categorized into further groups (mild, moderate, and severe) depending on the severity of their disease. Additionally, they included a test for memory for spoken material as well as music which was a development done due to a limitation found in their previous research study. They concluded that AD participants faced challenges when responding to the test instructions however was frequently able to indicate the familiarity and ability to recognize any distortion which was indicated through their behavioral gestures. As the previous findings and the findings from their current study correlated, this was quite helpful in establishing the reliability of not just their previous study but also their current. Their findings were similar to the findings of Janata (2007) paper mentioned above, that music had potential to evoke memory, Janata did focus on autobiographical memories whilst this study was more focused on whether participants could identify long-term familiarity for a melody. I think although this study shows the reliability of their previous study, and found that long-term familiarity was found for the melodies played, even though those across all levels of Alzheimer’s, it doesn’t provide insight into whether any past personal memories were experienced during these sessions. As it only shows the familiarity of a melody, this study could be used as background research for future studies like Janata, as this shows the possibility of Alzheimer patients were able to recognize familiar melodies and even to some extent identify melodic distortion.

Article 3- Music evoked autobiographical memory after severe acquired brain injury: Preliminary findings from a case series

Music is a unique stimulus that has the ability to evoke and enhance autobiographical memories and associated emotions. Samson and Baird’s (2014) study was the first to explore music-evoked autobiographical memories in patients with acquired brain inquiry (ABI). Being a pioneer in this field, their sample size was quite low, with 5 patients with severe ABI between 20-60 years of age. They had their patients complete an autobiographical memory interview followed by a standard neuropsychological assessment. They found that a vast number of MEAMs’ cases were of a person/people or a period of life. The results imply that music is a potent stimulus for evoking autobiographical memories. This experimental research was quite insightful as it builds upon the concept of MEAMs’(Janata et al., 2007), where MEAMs’ predominantly associated with positive emotions, resulting in confirming that music is a potent and useful stimulus for exploring the nature of autobiographical memories (Janata et al., 2007). Samsom and Braid also build on El Haj et al (2012) study which resulted in saying that these features of MEAMs were common with ‘involuntary autobiographical memories’. Concatenating these two studies together, formed Samson and Braid to the 4 sub-aims of this study, (1) to characterise the phenomenology of MEAMs in patients with severe ABI, (2) to investigate music evoked in contrast with verbal evoked autobiographical memories, (3) to explore the possibility of music to be used in rehabilitation of retrograde, specifically autobiographical amnesia, after ABI, and (4) to provide preliminary insights into the role of frontal brain regions in MEAMs The findings state that the frequency of MEAMs’ was similar for patients and those in the control group, the songs that evoked a memory were songs with a positive association behind them. This study did find that although ABI patients were able to enhance memory, a family member such as a wife, who lived through the same memory had a more clear and precise memory evoked. So although the patients were able to elicit a memory, it certainly was not to the same extent as a healthy- brain person. This research design is targeted to help those with ABI, professionals trying to help those with ABI try to reconnect with their sense of self and help ABI patients loved ones.

Conclusion

The three studies, all explored the connection between music and memory, specifically the majority targeted MEAMs’ of a patient with a cognitive disorder. Their age groups were quite similar, comparing young adults and the elderly at most times. Certainly, the strength of Janata et al (2007) research was portrayed through the other two pieces of research building on that article. The concept of MEAMs’ certainly opened many pathways for potential help for patients with Alzheimer’s or other acquired brain injury. Some limitations faced that were common throughout the three articles, was the struggle faced by the patients to understand the task at hand itself, but that didn’t necessarily prevent the authors from finding the results. Future studies could look into the connection of emotions and the memory, to help recognize the mechanisms that define the unique memory-enhancing effect formed from music(Baird & Samson, 2014). They could also investigate whether repetition over a longer period of certain music or melody helps develop a memory into a more precise version.

References

1. Baird, A., & Samson, S. (2014). Music evoked autobiographical memory after severe acquired brain injury: preliminary findings from a case series. Neuropsychol Rehabil, 24(1), 125-143. doi:10.1080/09602011.2013.858642
2. Barlett, J. C., Halpern, A. R., & Dowling, W. J. (1995). Recognition of familiar and unfamiliar melodies in normal aging and Alzheimer’s disease. Mem Cognit, 23(5), 531-546. doi:10.3758/bf03197255
3. Bartlett, J. C., & Snelus, P. (1980). Lifespan Memory for Popular Songs. The American Journal of Psychology, 93(3), 551-560. doi:10.2307/1422730
4. Crovitz, H. F., & Schiffman, H. (1974). Frequency of episodic memories as a function of their age. Bulletin of the Psychonomic Society, 4(5), 517-518. doi:10.3758/BF03334277
5. Cuddy, L. L., & Duffin, J. M. (2005). Music, memory, and Alzheimer’s disease: Is music recognition spared in dementia, and how can it be assessed. Medical hypotheses( 64), 229–235.
6. Cuddy, L. L., Duffin, J. M., Gill, S. S., Brown, C. L., Sikka, R., & Vanstone, A. D. (2012). Memory for Melodies and Lyrics in Alzheimer’s Disease. Music Perception: An Interdisciplinary Journal, 29(5), 479-491. doi:10.1525/mp.2012.29.5.479
7. Halpern, A., & Bartlett, J. (2010). Memory for Melodies. In (pp. 233-258).
8. Janata, P., Tomic, S. T., & Rakowski, S. K. (2007). Characterisation of music-evoked autobiographical memories. Memory, 15(8), 845-860.

Introduction

A little over a year ago, there was a sweet 90 year old woman at a nursing home. Her name was Analisa Caroler. During her stay at this nursing home, she used to tell the most amazing stories of her past. However, a year ago, she began showing signs of Alzheimer’s. She was shocked. 20 years ago, she discovered she carried a genetic marker for Alzheimer’s. Because no symptoms ever surfaced before she was 85, her doctors felt that her Alzheimer’s would never surface. Still, during these 20 years, she never knew if she was going to have Alzheimer’s or when she was going to begin showing symptoms. This was because she never received a thorough diagnostic test on her Alzheimer’s disease. Currently ranked as the sixth leading cause of death in the United States alone, Alzheimer’s disease is a serious condition that arises in someone in the United States every 65 seconds. Roughly 10 percent of adults are diagnosed Alzheimer’s after the age of 65 and at least 32 percent after the age of 80. More so, 25 percent of those originally diagnosed with Alzheimer’s are misdiagnosed, commonly due to the lack of a full diagnostic report and series of tests. The misdiagnosis is due in full to the insufficiency of appropriate testing for patients. Alzheimer’s is a heavily genetically influenced degenerative disease. With Alzheimer’s, there is one main genetic variant linked to the regression. This is the APOE gene. The APOE gene is responsible for the creation of the class of proteins called the Apolipoprotein. The Apolipoproteins produce proteins that cause the degeneration in the brain. However, detecting the abundance of Apolipoprotein can, currently, only be done two ways: PET scans and Spinal Taps, which are expensive and invasive, causing many patients to be dissuaded of getting a full diagnosis. Targeting the amount of Apolipoprotein from a simple blood sample from a patient to create a new diagnostic test can show the state of the Alzheimer’s in its degeneration, can be detected by a series of electrophoresis tests on the Alzheimer’s cell line, and can ease the vexatious uneasiness of those who are unaware of the progression Alzheimer’s disease in a patient. A full diagnosis of Alzheimer’s disease is necessary for doctors working on clinical trials, for patients unsure of the state of their disease, and for pharmaceutical companies looking for treatments and can be achieved by targeting the creation of a test that analyzes a patient’s blood.

Background Information

Alzheimer disease (AD) is a progressive neurodegenerative disease associated with cognitive decline and is the most common form of dementia in the elderly. Dementia is the loss of cognitive function – thinking, remembering, and reasoning – and behavioral abilities to such an extent that it interferes with a person’s daily life and activities[13]. Alzheimer’s is a progressive disease, where dementia symptoms gradually worsen over a number of years. In its early stages, memory loss is mild, but with late-stage Alzheimer’s, individuals lose the ability to carry on a conversation and respond to their environment[4]. It is the most common cause of dementia in older adults. Alzheimer’s Disease is a neurodegenerative disease that is heavily affected by genetics. There have been studies that have looked into family studies and twin studies to further the knowledge in how the biology of the genetics works. It has been discovered that the there are specific gene mutations that link directly to Alzheimer’s disease[12]. Alzheimer’s has no current cure, but treatments for symptoms are available and research continues. However, efforts are coming into play in order to carve a new path to finding treatment plans for patients.

Apolipoprotein role in Alzheimer’s

The abundance of Apolipoproteins can be measured from the patients blood and shows a direct correlation in the progression of Alzheimer’s. In an Alzheimer’s patient, the gene that is linked to Alzheimer’s lies within their genes. From a blood sample, the genetic variant tied to Alzheimer’s in a patient can be detected. Apolipoprotein E is a major cholesterol carrier that supports lipid transport and injury repair in the brain. APOE polymorphic alleles are the main genetic determinants of Alzheimer’s disease risk: individuals carrying the E4 allele are at increased risk of AD compared with those carrying the more common E3 allele. Presence of the APOE E4 allele is also associated with increased risk for cerebral amyloid angiopathy and age-related cognitive decline during normal ageing[11].

Effects of Alzheimer’s Disease on Patients

Alzheimer’s disease is an illness of the brain. It causes large numbers of nerve cells in the brain to die. This affects a person’s ability to remember things, think clearly, and use good judgment. People with Alzheimer’s disease have trouble doing everyday things like driving a car, cooking a meal, or paying bills. They may get lost easily and find even simple things confusing. Some people become worried, angry, or violent[15]. Alzheimer’s disease occurs when there is an accumulation of beta-amyloid or neurofibrillary tau tangles in the brain. AD is a heavily genetically influenced disease. With Alzheimer’s, there is one main genetic variant linked to the regression. This is the APOE gene. The APOE gene is responsible for the creation of the class of proteins called the Apolipoprotein E4. The Apolipoproteins produce proteins that cause the degeneration in the brain[14]. Human apolipoprotein E (ApoE) is associated with high cholesterol levels, coronary artery disease, and mostly in Alzheimer’s disease.

Effects of Apolipoproteins in Alzheimer’s Disease

The Apolipoprotein gene variant is very important an crucial in Alzheimer’s research. This gene variant only determines if the patient is more susceptible to getting Alzheimer’s disease. However, the amount of the beta-amyloid, the protein that causes Alzheimer’s, is what determines how far in the progression of Alzheimer’s a patient is[2]. Genome-wide association studies have confirmed that the ε4 allele of APOE is the strongest genetic risk factor for AD. The presence of this allele is associated with increased risk for both early-onset AD. The amyloid precursor protein gene is linked to the chromosomes 1 and 19. The targeted protein, Apolipoprotein E gene variant, has been reported to be located on the chromosome 19 for patients with late-onset Alzheimer’s In addition, it has also been discovered that the chromosome 21, the chromosome known for its association with Down Syndrome, is a candidate for Alzheimer’s genes. Those with Down Syndrome have a higher risk and link into getting Alzheimer’s disease[12].

Using An Electrophoresis Test

An electrophoresis test on an Alzheimer’s cell line should be able to detect Apolipoprotein abundance without being invasive or costly. After the cell line from an Alzheimer’s patient is isolated, the genetic variant tied to Alzheimer’s disease can be targeted and amplified. This amplification allows easy detection.

Presence of Apolipoprotein RNA in Exosomes

The presence of Apolipoprotein RNA in exosomes can show the regression of Alzheimer’s disease. In the brain, there are small vesicles secreted by neurons that function in intercellular communication called exosomes. These exosomes have been observed to play a role in spreading pathological misfolded proteins. In Alzheimer’s disease, there are two types of lesions: Amyloid plaques and neurofibrillary tangles. The role of exosomes in the metabolism and secretion of APP and Tau proteins and their subsequent impact on AD pathogenesis is studied in this review. The biogenesis and function of exosomes impact amyloidogenic processing and tau pathology. The exosomes have a “double-edged sword” effect on the progression of AD. The discovery of the path in which exosomes travel could provide insight into the diagnosis of AD and the platform to allow therapeutic drugs for AD[17].

Experimentation With Electrophoresis and Exosomes

The mutated cells are isolated and filtered to get rid of extremities. RNA strands from the specific cell line are isolated and amplified. This process is completed my using High-Capacity cDNA Transcription. RNA is converted into cDNA by using the technology, Reverse-Transcriptase Polymerase Chain Reaction (RT-PCR). This approach is used to study gene expression. Although RT-PCR and the traditional PCR process both produce multiple copies of particular DNA isolates through amplification, the applications of the two techniques are fundamentally different. Regular PCR is used to exponentially amplify target DNA sequences. RT-PCR is used to copy expressed genes by reverse transcribing the RNA that was extracted into cDNA (complement DNA) through the use of reverse transcriptase. Subsequently, the newly synthesized cDNA is amplified using traditional PCR. Therefore, instead of having an amplified target DNA sequence, we can look at the amplified cDNA sequence that was reverse transcribed from RNA[5]. Comparing the results from testing a mutated cell line and a non-mutated cell line to discover the presence of apolipoproteins in the cell line using electrophoresis tests, experimentation has proven to be successful in detecting exosomal presence in electrophoresis.

RNA Expression of Apolipoprotein in Blood Sample

Many people know that Alzheimer’s is a hereditary disease. However, what they don’t know is how it works and they there is a probable chance that it can even be transmissible through blood. A study has found that Alzheimer’s protein can spread between mice that share a blood supply, causing brain degeneration. Other diseases like Creutzfeldt-Jakob Disease (CJD) can spread through meat products or blood transfusions infected with prion proteins because they have misfolded proteins that are known to cause CJD. Like CJD, Alzheimer’s also has involves a misfolded protein called beta-amyloid. There has been recent evidence that beta-amyloid may be able to spread like the prions in CJD. A recent tried conjoining a healthy mouse and a mouse with Alzheimer’s plaques. They surgically attached the two mice in a way that made them share a blood system. The study proved to be truthful in the transference of those beta-amyloid proteins from the mouse with Alzheimer’s to the healthy mouse[9]. RNA transcriptome in AD can help the understanding of how the disease presents itself. The effects of white matter hyperintensities on AD blood transcriptome has not been considered. The RNA from whole blood was processed on whole-genome microarrays. It is suggested that blood-based biomarkers could be useful for evaluating diagnosis, pathogenesis and progression of AD. RNA expression in blood of patients with AD has been assessed in several recent independent studies.. The aim of this study was to examine RNA expression in blood of AD patients with and without WMH as compared to controls.The study shows that a number of the genes regulated in this study have been reported to be regulated in other studies of both AD blood and AD brain, and strongly support a systemic effect of AD that includes altered RNA expression of peripheral immune cells. Further validation in an independent cohort to specifically test the sensitivity and specificity of the identified genes to predict AD is needed[3].

Purpose For Finding An Alternative Diagnostic Test

Finding an alternative form to testing for Apolipoprotein abundance in patients is necessary because it allows for more effective treatment procedures. For the 113 years since Alzheimer’s disease was discovered, neither a treatment nor a cure has been found. This absence of a treatment for Alzheimer’s has many negatory costs.

Benefits for Patients

Sandra Day O’Connor, the first woman on the Supreme Court, announced Tuesday in a frank and personal letter that she has been diagnosed with ‘the beginning stages of dementia, probably Alzheimer’s disease.’O’Connor said doctors diagnosed her some time ago and that as her condition has progressed she is ‘no longer able to participate in public life.’ After her 2006 retirement from the high court O’Connor had appeared around the country championing an educational organization she founded and serving as a visiting appeals court judge, among other activities. But she stopped speaking publicly more than two years ago. Her Alzheimer’s was not diagnosed until she began showing symptoms of dementia[16]. However, finding a new diagnostic test does not just benefit people like Sandra. Since Bill Gates announced his investment in research on Alzheimer’s disease, he received widespread appreciation and support. When asked on the reason behind his newfound support, Gates revealed that it was because his father, Bill Gates Sr. suffered from Alzheimer’s disease. Gates further explains that the reason with no cure found for Alzheimer’s yet is because it is a chicken-and-egg issue. Without an accurate, precise, painless, and non-costly form of diagnosis, Alzheimer’s will be unable to be treated or cured. Because of this, Gates invests more than $30 million towards the project, Diagnostics Accelerator, of the Alzheimer’s Drug Discovery Foundation[7]. Finding an alternative testing allows for closure from patients. At age 49, a woman by the name of Julie Gregory paid an online service to sequence her genes. She was not originally looking for it, but soon found out that she had two copies of the ApoE4 gene. This gene is strongly linked to Alzheimer’s. Many scientists say that there is no other way to detect whether you have dangerous plaques that are known to cause Alzheimer’s unless you get a $4,000 PET scan or an extremely painful spinal tap. While genetic tests can help predict risk of getting the disease, it is still unable to reveal the state of the disease in your brain. Many people will go years without ever showing a single sign of Alzheimer’s even if they had it. Another woman, acknowledged as D., also found out about her ApoE genotype. After finding out, she, like many upon finding out, began to have the looming thought/ question about when and if she would be getting Alzheimer’s. The biggest fear with knowing that someone carries the ApoE4 gene variant is that those people would never know what state the disease is at in their head, when they would begin showing symptoms of the disease, and how bad the disease can get. The big issue is that people in the early stages of Alzheimer’s will never know unless they got tested[10].

Benefits for Researchers and Pharmaceutical Companies

Alzheimer’s disease is expected to increase prevalently in the near future. As of now, there is no definitive diagnosis process that can determine the state of the Alzheimer’s progression in a patient with ease in accuracy and precision. Many patients are incorrectly diagnosed. Cerebrospinal Fluid biomarkers have been discovered to be the closest thing to getting an accurate diagnosis. However, just like many things on this earth, CSF has its flaws and is difficult to obtain. Although these CSF biomarkers have supported the identification of tau tangles in the brain, the performance in giving an appropriate diagnosis is still at risk because it only gives a moderate diagnosis. It is also possible that when running labs on the CSF, it was frozen throughout the duration in order to preserve the biomarkers, which could have caused error in the process[8]. Out of all dementia cases, roughly 6o to 80 percent of these cases are Alzheimer’s disease. The number of cases introduced each year is ever increasing. Nearly every 66 seconds, there is a new case of Alzheimer’s introduced. There are fairly effective psychiatric medication options for the anxiety that comes with living with constant confusion. There are three main reasons that scientists have not discovered a drug to treat Alzheimer’s disease, among them being that there is 25% chance that the patients in clinical trials where these drugs are tested have, in fact, been misdiagnosed with Alzheimer’s[6].

Conclusion

In the last 113 years, since Alzheimer’s disease was discovered, no cure or treatment plan has been procured. An alternative to accurately and precisely diagnosing Alzheimer’s disease is a necessary advancement in medicine because it affects a large portion of the current population. The amount of Apolipoproteins in a cell line from a patient can help to determine the presence of the Alzheimer’s and its position in the pathway to degeneration of a patient’s brain, as well as, help patients gain closure for their disease, even if there is not cure discoverable. Although current Alzheimer’s treatments cannot stop Alzheimer’s from progressing, they can temporarily slow the worsening of dementia symptoms and improve quality of life for those with Alzheimer’s and their caregivers. Today, there is a worldwide effort under way to find better ways to treat the disease, delay its onset, and prevent it from developing.

Introduction

This review will be investigating how poor dental hygiene can be a risk factor for Alzheimer’s disease (AD). AD is a progressive brain disorder that results in a decline in cognitive functions such as thinking, memory and behaviour (Holmer et al., 2018). It is the most common type of dementia (Gaur & Agnihotri, 2015) and is categorised into 3 main stages: mild, moderate and severe. A hallmark for the disease is brain inflammation (Rogers, 2008) and the presence of beta amyloid plaques in the brain and neurofibrillary tangles made up by hyperphosphorylated tau proteins. These plaques are sticky aggregates of amyloid precursor protein (APP) that can be neurotoxic. The plaques and tangles can cause a disruption in the supply of nutrients to brain cells resulting in neuron cell death and a decline in cognitive function which can lead to AD (Rogers et al., 1988).

The development of AD can be caused by many factors such as age, genes and environmental factors (Liu et al., 2019). One of the possible risk factors can be poor dental hygiene. This article is going to discuss research looking into the relation between these two factors and how one might cause the other. Alzheimer’s is most common in elderly patients (Rogers, 2008) and there can be bacterial, fungal and viral causes. This review will be focussing on the elderly population and looking into the bacterial causes of AD.

Beta amyloid plaques and Neurofibrillary tangles in Alzheimer’s Disease

The beta amyloid plaques in the brain are thought to trigger neurodegeneration which can cause Alzheimer’s and so it could be assumed that there would be more plaques in the brain of an AD sufferer. This is supported by (Kamer et al., 2009). These beta amyloid aggregates and neurofibrillary tangles would specifically be found in certain areas of the brain that are affected by AD and this is supported by a study that shows that they were found in areas such as the limbic system and the frontal neocortex (Rogers, 2008) which are responsible for cognitive skills such as memory, judgement and problem solving (Kunst et al., 2019). These are the skills that can be known to deteriorate during progression of Alzheimer’s so the presence of the aggregates and tangles here suggests they could play a part in the pathogenesis of the disease.

These plaques and tangles cause neuroinflammation by forming beta-pleated aggregates that are surrounded by microglia cells. These cells can be activated by the presence of beta amyloid plaques and neurofibrillary tangles as a CNS response to prevent neurodegeneration. As a result, the microglia cells can release inflammatory mediators and when activated and cause neuroinflammation.

Bacteria found in the brain can trigger these microglia cells so that they become activated. Overstimulation of microglia cells can cause harmful neuroinflammation and neurodegeneration through the release of cytokines and neurotoxic substances such as free radicals which cause neuron cell death (Olsen & Singhrao, 2015).

Oral microbiota dysbiosis in AD

Poor dental hygiene can result in caries and periodontal disease which can cause dysbiosis of the oral microbiota. Periodontal disease can result in, gram-negative, anaerobic bacteria such as Porphyromonas gingivalis and Treponema denticola (also known as keystone pathogens), dominating under the low bioavailability. This decreases the overall species richness and diversity of the oral microbiota (Harding et al., 2017). This is supported by a study that analysed the saliva samples of AD patients and found that the bacterial populations had a lower species diversity and richness in patients with AD than in non-AD patients. Another study that reflects this used the sequencing of 16s rRNA and also found that those with AD had a lower diversity of microbiota. This further supports the idea that the constituents of the oral microbiota can cause or affect the development of Alzheimer’s (Liu et al., 2019). Both of these studies are very recent and there is not much data backing up the findings so further experiments could have different results. More evidence would be needed to draw a strong association between constituents of the oral microbiota and the progression of AD.

This dysbiotic flora can over-activate the inflammatory response and cause periodontal tissue destruction leading to the release of many inflammatory mediators and an increase in the number of harmful bacteria in the oral tissues. The inflammatory mediators and bacteria can travel to the brain after entering the blood stream through bacteraemia. Methods of bacteraemia can be through daily actions such as brushing your teeth and chewing (Allen, 2010). The inflammation and dysbiosis positively reinforce each other as inflammatory tissue breakdown products are used as nutrients by the dysbiotic microbiota, which will result in neuroinflammation and neurodegeneration. Figure 1 shows the effect of oral bacteria in the brain on neuronal cells.

The presence of poor dental hygiene associated bacteria in the brain of AD patients is a factor supporting the theory that there is an association between poor dental hygiene and AD development. A very recent study found certain periodontal bacteria such as Trepenoma denticola in brain tissue of patients with Alzheimer’s (Riviere et al., 2002). This can suggest oral bacteria can travel to the brain and trigger the neuroinflammation although the extent to which these bacteria effect the severity of the disease is still being looked into. It can be suggested that particularly spirochete bacteria such as Trepenoma denitcola can cause Alzheimer’s as spirochetes were found in 14/16 of the brains of patients with AD using varying techniques (Riviere et al., 2002) (Miklossy, 2011) and it was found that they produced beta amyloid plaques in the brain which is a hallmark for AD (Miklossy et al., 2006).

Association between peripheral inflammation and AD

Neuroinflammation can be caused by proinflammatory mediators travelling from an area of peripheral infection to the brain. (Kempuraj et al., 2020). Poor dental hygiene can lead to a build-up of plaque which can cause gum disease and periodontitis – a form of peripheral infection (Marchini et al., 2019). Periodontitis is an oral infection that can produce inflammatory mediators, virulence factors and result in an increase in harmful bacteria that can travel to the brain through the bloodstream. Peripheral infections can increase the permeability of the blood brain barrier and so it is easier for these pathogens and mediators to reach the brain. The bacteria can result in activation of microglia cells which can release neurotoxic substances such as free radicals that cause neuron cell death (Riviere et al., 2002). The microglia cells can also cause the formation of beta amyloid plaques and tau protein hyperphosphorylation in the brain which causes neurodegeneration and activates further microglia cells.

Oral bacteria and the brain

Bacteria can also enter the brain through parts of the vascular system not involving the BBB such as the choroid plexus. In the brain, microglia cells can use their CD14 receptors and Toll-like receptors (TLRs) to recognise LPS (Lipopolysaccharide) of the bacteria (Lacroix et al., 1998). When bacteria enter the bloodstream, the innate immune system is activated by the recognition of PRR (pattern recognition receptors) and TLRs (toll like receptors) (Dunn et al., 2005). The TLRs release cytokines into the bloodstream which can cause the release of secondary mediators that can cause neurodegeneration in the brain (Holmes et al., 2003). Furthermore, periodontitis can precede other health conditions such as atherosclerosis and other inflammatory disease in the systemic system (Pischon et al., 2007). This can result in further inflammatory mediators in the bloodstream that can travel to the brain and contribute towards further neuroinflammation.

Immune responses to oral bacteria in the brain

Antibodies related to bacteria involved in periodontal disease such as Porphyromonas gingivalis are found in patients who suffer from AD and can be evidence towards the link between the disease and poor dental hygiene. Kamer et al. (2009) found that those with AD had a higher level of specific antibodies against certain periodontal pathogens. This study only involved 34 subjects which is a relatively small sample size and is not be representative of the whole population. Furthermore, all of the subjects were selected from New York University and so the results can only be representative of that area. Furthermore, the level of antibodies found may vary based on the different severities of AD and so these results would not reflect that. However, from the data that was found, we can assume that bacterial populations that become more common in the oral microbiota of a patient with poor dental hygiene could travel to the brain and cause neurodegeneration. The release of antibodies against these bacteria is a defence mechanism to try and kill the bacteria hence we can look at these specific antibodies to tell us that pathogenic oral bacteria is present in the brain.

The complement pathway may also cause an increase in the severity of AD and can be activated by poor dental hygiene. C1q is a protein which acts as a component of the complement activation pathway. It can be found in patients who suffer from AD. It is thought that C1q may have a role in Alzheimer’s as the complement pathway is known to increase inflammation (Fonesca et al., 2004). In a study, mice with and without C1q were observed and it was found that both the mice had beta amyloid plaques present however, in the mice without C1q, there were less microglia cells accumulated around the plaques than in the mouse with C1q. This can suggest that the presence of C1q allows the complement cascade to be activated in the brain of an AD patient and that this can contribute towards the neurodegeneration in the disease. This study is quite old but is supported by a more recent study by Hajjshengallis G et al. (2019) which is very popular and found that there can be hyperactivity of the complement cascade during periodontitis which can result in inflammatory mediators being released that can travel to the brain and cause neuroinflammation . Since one of the main causes of periodontitis is poor dental health, we can draw the assumption that poor dental health can result in activation of the complement cascade which can go onto increase the rate of progression of Alzheimer’s (Hajishengallis, 2015). In support of this, (Emery et al., 2017) found that complement can be activated by oral bacteria.

Inverse effect of AD on poor dental hygiene

Poor dental hygiene could be a risk factor for Alzheimer’s, but the progressive cognitive decline may also result in a deterioration of dental hygiene which can create a cycle in which both get progressively worse. In the severe stage of AD, the patient will most likely be reliant on their caregiver to manage their oral hygiene. A caregiver will also be responsible of taking care of them in other ways due to their loss of functionality and so oral hygiene may not be a priority and therefore, may suffer (Marchini et al., 2019).This can further have a detrimental effect on both your oral health and the severity of neurodegeneration. A study that shows that oral health care in some institutions is not seen as good is (Yoon et al., 2018). However, this study was conducted in Canada and cannot be representative of care homes everywhere, the results may vary country to country.

Conclusion

There is a strong association between poor dental hygiene and the development of AD as there have been studies that have found periodontal related oral bacteria in the brain of Alzheimer’s patients and linked this to activation of microglia cells and the complement system, hyperphosphorylation of tau proteins and accumulation of beta amyloid plaques; all of which can cause neuron cell death. Furthermore, patient’s with later stages of Alzheimer’s have decreased functionality and so their dental hygiene suffers even more which can cause the Alzheimer’s to the progress further. However, there is still a lack of research with regards to this topic and although we can predict a strong association between the two factors, there is further scientific research needed to strengthen the currently existing evidence.

Imagine going home and seeing your father forget on how to tie his shoe, forgetting how to cook toast, or even solving a simple math problem and getting frustrated at himself for failing. You start to notice the signs of dementia, but you think he’s only 50? You do some research and realize he has Early-Onset Alzheimer’s. You take him to the doctor and find that it’s all true. You’re terrified and don’t know how to help or even where to start.

What is Early-Onset Alzheimer’s? “Early-Onset Alzheimer’s is an uncommon form of dementia that strikes people younger than age 65” (Graff-Radford,2017). In Reference to the Alzheimer’s disease genetics fact sheet, Alzheimer’s is caused by three different single-gene mutations on the chromosomes 1, 14, and 21. The mutations on each of these genes cause proteins to be formed. The mutation on chromosome 1 leads to abnormal Presenilin 2, mutations on chromosome 14 causes abnormal Presenilin to be made, and finally mutations on chromosome 21 cause the formation of abnormal amyloid precursor protein (APP) (NIH, 2015).

When having Early-Onset Alzheimer’s it’s important to know the symptoms so you can start to recieve help. According to the Alzheimer’s association some signs include memory loss that disrupts daily life this includes forgetting recently learned information. Another symptom is challenges in planning or solving problems, this includes learning recipes and working with numbers. Another symptom is difficulty completing familiar tasks at home, at work or at rest. Next is confusion with time or place, or even trouble with understanding visual images and spatial relationships. New problems with words in speaking or writing, misplacing things and losing the ability to retrace steps, decreased or poor judgement, changes in mood and personality, and finally withdrawn from work or social activities, It’s important to know the signs of Early-Onset Alzheimer’s to protect yourself and your loved ones.

Five percent of people who have Alzheimer’s disease experience the symptoms before age 65. In America about 200,000 people have early-onset alzheimer’s disease. The symptoms for early-onset would begin around your 40s and 50s (Graff-Radford, 2017). Early-onset affects those younger than age 65. Recent studies have shown that female Latinos and African Americans have a higher risk of early-onset alzheimer’s. Hypertension, diabetes, strokes, and coronary artery disease are all risk factors for Alzheimer’s. These conditions are more common in Latinos, and African Americans compared other Americans.(US Against Alzheimer’s).

According to the U.S National Library of Medicine, Alzheimer’s is an autosomal dominant. This means that one copy of an altered gene in each cell is sufficient to cause the disorder. This usually occurs when an affected parent gives its offspring an altered gene (U.S National Library of Medicine, 2019).

Diagnosis is essential to truly figure out if you have early-onset Alzheimer’s. According to the Alzheimer’s Association, you will need to be evaluated by someone who specializes in alzheimer’s. From there the diagnosis would consist of a medical exam, cognitive tests which test memory, language, skills, math, and problem solving skills. Neurological exam or brain imaging. Neurological exams asses balance, sensory response, reflexes and electroencephalogram which check for abnormal brain activity. The Alzheimer’s Association states “keep in mind there is no one test that confirms Alzheimer’s disease. A diagnosis is only made after a comprehensive medical evaluation” (Alzheimer’s Association,2019). Sometimes for early-onset genetic testing can show increased risk for early-onset. This gene is APOEe4 (Mayo Clinic Staff,2018).

What are the treatments for early-onset Alzheimer’s? Well actually there is no cure Early-Onset Alzheimer’s or medication that could stop or slow the progression. However, ‘there are drug or non-drug options that may help treat the symptoms. Understanding available options can help individuals living with the disease and help improve quality of life.”(Alzheimer’s Association, 2019) One option is medications for memory loss. Drugs used to help early stages are cholinesterase inhibitors. These drugs are used to help treat symptoms for memory, language, thinking, judgement, and other thought processes. They also help prevent the breakdown of a chemical called acetylcholine, which is used as a messenger that is important for memory and learning that supports communication among nerve cells by keeping acetylcholine high. Other ways for treatment are behavioral medications and the use of caregivers. With the help of the Alzheimer’s Association some new promising targets for next generation drug therapies are being studied in recent investigations. The first one is Beta-amyloid and it is a chief component of plagues, one hallmark alzheimer’s brain abnormality. Scientists have newly detailed information of how the protein fragment is clipped from its parent compound, APP, by two enzymes known as Beta-secretase, and Gamma-secretase. Together they form the Beta-amyloid protein, which is present in abnormally high levels in the brains of people with Alzheimer’s. Since the information is now known, researchers have began developing medications that are aimed at every point in the amyloid processing pathway. The current drug that targets Beta-amyloid is Aducanumab and it is a recombinant monoclonal antibody targeting aggravated forms of Beta-amyloid. Another enzyme that clips is Beta-secretase. Beta-secretase makes it possible for Beta-amyloid to form and with therapies, hopefully be able to reduce the amount of Beta-amyloid and interrupt development of Alzheimer’s. The drug for this is JNJ-54861911, and it inhibits the ability of Beta-secretase to make Beta-amyloid. There are many more treatments, drugs, and therapies being tested and researched in hopes of finding a cure. (Alzheimer’s Association, 2019)

Alzheimer’s disease was first discovered in 1906 by Dr. Alois Alzheimer. However, it is not known when the early form was first recognized. Dr. Alois Alzheimer first noticed changes in the brain tissue of a women who died of an unusual mental illness (NIH,2016). The cause of Early-Onset Alzheimer’s is still unknown besides the genetic mutations on chromosomes 1,4,and 21. A new clinical study The Longitudinal Early-Onset Alzheimer’s disease study. It is a non-randomized, natural history, non-treatment study that is designed to look and observe at the disease progression in individuals with Early-Onset cognitive impairment.

There are many organizations and support groups for those who are affected with Early-onset Alzheimer’s. The Alzheimer’s association has many resources for help.They have a 24/7 helpline, local offices and programs, education programs, social engagement programs, and online tools. Those were some support groups for those with Early-Onset but there are also some for the friends and family.Counseling, therapy, and support groups are essential to maintain a healthy mental health for friends and family of those who have Early-Onset Alzheimer’s. Locally, here in Wichita kansas, the Alzheimer’s association building hosta classes, groups, and will always be there to help.

Early-Onset Alzheimer’s is rare in the united states compared to the common late Alzheimer’s. As a result of Alzheimer’s being so common there are some celebrities who had a form of dementia and Alzheimers. Rosa parks was diagnosed with dementia in her late years of life. Another famous person was Ronald Reagan. Regan was diagnosed with alzheimer’s in 1994, only 5 years after leaving the office. Besides celebrities who had a form of demita, there were also some who helped promote the awareness. Seth Rogen lost his mother due to Early-Onset Alzheimer’s. His mother was diagnosed in her 50s. After that Seth and his wife decided to create a charity called Hilarity for Charity. This charity was an educational campaign to teach younger people about Early-Onset Alzheimer’s in hopes to reduce the stigma of it (Sauer,2016). Finally, to promote the disease, The Alzheimer’s association plans and creates a walk for the awareness of Alzheimer’s.

After finding out all of the information about Early-Onset you start to relieve your stress and know how to help your father. You learn about medications and therapies to help with the symptoms. You learn about the best way to help him and you learn more about how it’s caused. You find support groups to help him and you finally, you understand what is happening and are able to take it all in.

In the exploration of pathogenesis of Alzheimer’s disease, many studies have revealed the origin of the disease and the underlying cause of its deterioration. For a long time, we have known that pathological changes in the brain of patients with Alzheimer’s disease, such as the accumulation of amyloid plaques, occurred before the onset of symptoms such as memory loss.

A new study published in Communications Biology by neuroscientists from the Massachusetts Institute of Technology provided new insights into the accumulation mechanism of the amyloid plate in the mouse brain. The study showed that the degree of amyloid accumulation in the relevant regions of the human brain is closely related to the worsening of the disease. Using a brain labeling technique called ‘SWITCH’, the researchers fine-tuned the brains of mice at different ages and found that plaques first appeared in deep brain structures such as the papillae, lateral septum and hypothalamus areas of equal depth in the brain, then spread along specific brain circuits within 6 to 12 months, and eventually enter the hippocampus (a key area of memory) and the cortex. In addition, according to a study published by the journal Cell, researchers from the Massachusetts Medical College found that genetic mutations trigger a mutation in a protein called ‘ataxin-1,’ which is likely to regulate the activity of beta-amylase and thus increase an individual’s risk of developing Alzheimer’s disease.

In an article published in the journal ‘PNAS’, researchers from Binghamton University and the University of Colorado have jointly drawn a structural map of ‘amyloid’ aggregates. In this study, the authors used high-resolution solid-state nuclear magnetic resonance spectroscopy to study these fibrous structures. Their work revealed that these fibers may have mutated in the molecular structure of the human brain’s amyloid deposits. This may be the cause of the disease.

In a study published in the journal Science, researchers from the Technical University of Munich, Germany, found for the first time that the excitatory neurotransmitter glutamic acid persisted for too long near active neurons. This causes these neurons to suffer from pathological overstimulation, which is likely to be a key factor in the loss of learning and memory in patients with Alzheimer’s disease. As we all know, neurons use chemicals called ‘neurotransmitters’ to communicate with each other. As one of the most important chemicals, glutamic acid plays a role in activating adjacent neurons. Researchers have found that under the action of beta-amyloid molecules: glutamate is difficult to transport out of the synaptic space normally. Therefore, high concentrations of glutamic acid persist in the synaptic space of highly active neurons for too long, resulting in excessive stimulation intensity. They tested similar mechanisms using beta-amyloid molecules from patient samples and tested them with various mouse models, all with similar results.

In an article published in the journal Cell Reports, researchers at the University of California, San Diego (UCSD) School of Medicine used transcriptomics to compare information on 414 patients clinically diagnosed Alzheimer’s. Finally, a map of gene-protein interactions was drawn. The authors believe that combining protein interactions with gene interference activities can provide a comprehensive framework for describing changes in related molecular networks during the onset of Alzheimer’s disease. Similarly, another study was published in the journal Neuron. In this study, researchers from Massachusetts General Hospital revealed the mechanism of interaction between CD33, a key gene of patients’ brain pro-inflammatory response, and the anti-inflammatory gene TREM2. It also emphasizes the role of the interaction between the two in the origin of Alzheimer’s disease. In another study published in the journal Nature Communications, researchers at the Center for Brain Science at the Japan Institute of Physics and Chemistry revealed the role of a gene called CAPON in regulating the pathogenesis of amyloid plaques and tau protein.

A study published in the journal Nature Neuroscience established a link between Alzheimer’s disease and cellular autophagy. In Alzheimer’s as well as other dementias, the accumulation of proteins tau and beta amyloid in the brain is responsible for cell death. In a new animal model, researchers have shown that the rate of this accumulation process slows as mitochondrial autophagy activity increases. Another study, also published in the journal Nature Neuroscience, revealed the causes of cerebral ischemic symptoms in Alzheimer’s patients. The authors found that the inflammatory response in patients’ brains led to the accumulation of neutrophils, which in turn triggered the clogging of capillaries in the brain and eventually results in reduced blood flow and the appearance of ischemic symptoms. In a study published in the journal Science, researchers from the Washington University School of Medicine found that lack of sleep increases the level of tau, a key protein in Alzheimer’s disease. In this study, the researchers inoculated tau protein clumps into the hippocampus of a group of mice, and then kept those mice awake for a long time each day. Another group of mice also received tau tangle injections, but was not forced to stay awake. After four weeks, the tau tangles spread farther in mice that lacked sleep compared to resting mice. These findings suggest that insufficient sleep helps to promote Alzheimer’s, and good sleep habits may help keep your brain healthy.

Reference:

1. Benedikt Zott et al., A vicious cycle of β amyloid–dependent neuronal hyperactivation. Science, 2019.
2. Evandro F. Fang et al., Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease. Nature Neuroscience, 2019.
3. Jaehong Suh,Donna M. Romano,Larissa Nitschke,et al., Loss of Ataxin-1 Potentiates Alzheimer’s Pathogenesis by Elevating Cerebral BACE1 Transcription, Cell (2019).
4. Jean C. Cruz Hernández et al., Neutrophil adhesion in brain capillaries reduces cortical blood flow and impairs memory function in Alzheimer’s disease mouse models, Nature Neuroscience (2019).
5. Rebecca Gail Canter,et al.,3D mapping reveals network-specific amyloid progression and subcortical susceptibility in mice. Communications Biology, 2019; 2 (1)
6. Saranya Canchi et al., Integrating Gene and Protein Expression Reveals Perturbed Functional Networks in Alzheimer’s Disease， Cell Reports (2019).
7. Shoko Hashimoto et al., Tau binding protein CAPON induces tau aggregation and neurodegeneration, Nature Communications (2019).
8. Zhi-Wen Hu et al., Molecular structure of an N-terminal phosphorylated β-amyloid fibril, Proceedings of the National Academy of Sciences (2019).

Are dogs really a man’s best friend and important? In many ways, dogs are important. This is because many dogs positively influence people with diseases or with a disorder. Relationships between dogs and humans are important because dogs can help people with Alzheimer’s disease, cancer, and autism spectrum disorder.

To begin with, many studies have proven that dogs impact people with Alzheimer’s by decreasing their amount of agitation and stress. Alzheimer’s disease is a brain disorder that ruins or slows memory and thinking skills. The main symptoms are memory loss, language problems, odd behavior, and agitation. According to an article by Linda Childers, a husband of a patient explained to her that putting the dog on his wife’s lap, who is affected by Alzheimer’s, calms and relaxes her. Dogs also help patients with Alzheimer’s by improving their mood. For example, many patients who are anxious or frustrated feel relieved and happy when having a dog by their side. A companion dog can also improve the quality of life for patients with Alzheimer’s. According to Catherine Travers, a center for research in geriatric medicine, an evaluation was conducted with 55 people affected by Alzheimer’s for 11 weeks. Each participant was given a dog and those conducting it recorded data over the weeks. The conductors saw a significant improvement in the participant’s quality of life and mood. In essence, dogs are very calming for those with Alzheimer’s.

In addition, dogs can help people with cancer by relaxing them. Cancer is a name given to a collection of related diseases; the body’s cells spread into surrounding tissue for all types of cancer. As well, dogs lower the patient’s blood pressure. Hospitals are now noticing the positive effect of dogs and are beginning to incorporate dogs in treatments. When the patient is going to therapy, a companion dog is brought with them to help them share their feelings and thoughts with their therapists. Dogs are extremely helpful during therapy for those with cancer. In fact, dogs help relax the patient and help them relieve all their anxiety and stress. Not only are dogs effective while therapy, dogs also can detect cancer. Dogs can detect cancer because there is a certain scent that they smell. Scientists have found some types of cancers dogs can detect. Some of these types of cancer are colon cancer, prostate cancer, breast cancer, and melanoma. To sum up, dogs are sufficient for those with many types of cancer.

Furthermore, dogs are beginning to help those with autism spectrum disorder in numerous ways. Autism spectrum disorder is a developmental disability, it can cause social, communication, and behavioral difficulties. Dogs benefit people with autism by improving their social awareness and behavior. In addition, a companion dog can increase their interactions with others and their motivations to do things. According to HARBI’s research in autism, a family who has a child with autism has a significant increase in family functioning compared to a family without. As well, dogs can decrease a child’s social isolation. They can do this by giving company to a child who may be isolated or alone. Children with autism become more responsive after spending time with a dog. This is because a dog can help them feel more outgoing and comfortable with others. Dogs also can give off a calming attitude and help the others around them feel the same, meaning, that dogs have the same effect on children with autism. Overall, autism is constantly influenced by dogs and their kind behavior.

In conclusion, dogs can help people with Alzheimer’s, cancer, and autism. Dogs truly help with their agitation and stress and play an important role in their day-to-day life. Relations between dogs and humans are extremely effective and crucial to those impacted by Alzheimer’s, cancer, and autism. We should all help and continue to get more hospitals to incorporate dogs.

Alzheimer’s disease (AD) is a mental health condition that associates with neurodegeneration and a decline in cognition making its victims lose memory, language capabilities, and praxis. With memory loss, AN individual loses THE ability to recall names, faces, and becomes out of touch with their emotional abilities. The condition affects individuals WHO ARE 65 years and above and with its widespread, the individual encounters personality alterations as well as increased and progressive loss of neurons with senile plaques becoming present. The same THING HAPPENS with their neurofibrillary tangles. Tremendous destruction takes place in their neural network, brain, and evident hippocampal atrophy. AD’s prevalence doubles after every five years and as the individual ages further, the prevalence generates an increase in time dependence exponentially. Nonetheless, AD is not prevalent among all the elderly and several other factors have been associated with normal aging.

My grandfather is one such victim and in his case, he started by forgetting many things, he has developed a tendency of doing harmful things to himself and this makes it harder to live with him. At times, he tries to escape the house because of the delusional thoughts of being somewhere else rather than at his house. His appetite is lost and it has become harder to let him take his medicines. Further, he has sleeping problems because of the negative thoughts that keep running through his mind. In my desire to understand why, my critical thinking led me to psychology in an attempt to understand why my grandfather has been having these experiences. Going through the textbook, I came across three chapters that helped me comprehend my grandfather’s behavior, in chapter 7, topics 2 and 3 on forgetting and biological bases of memory, in chapter 2, topic 4 on the cerebral cortex and in chapter 5, topic 2 on understanding sleep and dreams.

In chapter 7, topic 3 on biological bases of memory, I came to the understanding that when an individual suffers from AD, THEY become predisposed to memory loss. The cause comes from the alteration of the brain’s neural networks that are responsible for synaptic and neurotransmitter functions of the brain. Like various other mental diseases, AD interferes with the physiology of the nervous system and the brain eventually disrupting the memory process. Alzheimer’s has been known not to attack all memory types with the same measure, what it’s associated with is the extreme decline in declarative/explicit memory that limits an individual’s ability to recall personal life experiences, information, and facts. Mainly, the affected area of the brain is the hippocampal formation that controls the sequence of events. However, a possibility exists among the people suffering from AD that they retain part of non-declarative/implicit memories making them classically accustomed to procedural tasks and conditioned responses.

Chapter 7 topic 3 leads into another important psychological relationship between AD and memory loss, topic 2 on forgetting. In the latter topic, based on Ebbinghau’s original research, forgetting can be caused by several reasons, and with respect to my grandfather, amnesia happens to be the reason why he no longer remembers his personal life experiences, information, and facts. Research on amnesia has shown people with memory loss tend to recall the negative feeling and this resonates well with MY grandfather as the negative feelings in his mind influence the way he relates with us and WITH HIS sleepING.

In chapter 2, topic 4, the frontal lobes have three distinct roles to play in the memory process. This comes in addition to its receptive and coordination of messages from every other lobe in the brain. The frontal lobe also produces speech in Broca’s area, instigation of voluntary movement through the motor cortex, and higher functions such as self-awareness, motivation, and creativity, among others. My grandfather’s Alzheimer’s case has interfered with the way his higher functions and with this, the way he reasons and the way he perceives himself has changed interfering with his normal brain functionality. That is the reason why MY grandfather seems to believe that escaping the house would lead him to somewhere else he has come to consider as his. It is important to understand that recognizing one’s brain is recognizing self because one becomes familiar with THEIR thoughts, personality, and everyday experiences. Sadly, MY grandfather no longer seems to recognize his brain and with this, he is failing in recognizing who he is, who he loves, where he lives, and what he does.

In chapter 5 topic is ABOUT understandING sleep and dreams, circadian rhythms, and sleep, in all creatures have been defined by the planet’s cycle of days and nights. The suprachiasmatic nucleus (SCN), a part of the hypothalamus controls how an individual perceives light and dark information in the brain. With this, messages are then sent to the pineal gland that releases melatonin causing sleep. In the case of MY grandfather, he has become a victim of poor sleeping patterns that interferes with the way he sleeps. While part of his sleep interference associates with the negative thoughts he has, he no longer sleeps like he is supposed. That means MY grandfather has a problem within his brain that limits the way his pineal gland releases melatonin causing him to sleep on time. The sleep problems encountered by MY grandfather have caused him to experience reduced motor and cognitive performance and this makes it easy to understand why he has become lazy lately. Also, this has interfered with his moods and is the reason why he has become irritable. Sleep deprivation is known to increase other illnesses and the lack of it can be associated with the reason grandfather’s Alzheimer’s has increased over time.

Alzheimer’s disease is a mental condition and its presence, LIKE any other mental condition influences the way its patient recall their life experiences and live daily. The case of my grandfather has been associated with memory loss contributed to by an alteration of the brain’s neural networks that are responsible for synaptic and neurotransmitter functions of the brain resulting in his predisposed memory loss. As shown on topic 2 on forgetting, amnesia also results in loss of memory associated with the recall of negative feelings affecting MY grandfather’s personal life experiences, information, and facts. MY Grandfather’s AD case has interfered with the way his higher functions and the way he reasons and the way he perceives himself has changed interfering with his normal brain functionality. With this, his sleeping patterns have also been interfered with and he no longer sleeps his required number of hours because of the negative feelings he harbors in his mind.

My sources came from personal experience and the following chapters from the textbook:

• Chapter 2 on neuroscience and biological foundations, topic 4 on the cerebral cortex
• Chapter 5 on states of consciousness, the topic understand sleep and dreams
• Chapter 7 on memory, topic 2 on forgetting
• Chapter 7 on memory, topic 3 on the biological bases of memory