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The most common neurodegenerative disease worldwide is Alzheimer’s and impacts millions of people. This neurodegenerative disease is irreversible and there is currently no known cure: there are only palliative treatments to slow down ever worsening symptoms. The first discovery of Alzheimer’s disease was in 1906 by Dr Alois Alzheimer. It is primarily known for its most obvious symptom of memory loss caused by abnormal changes in the structure of the brain and for this reason is categorised under the broad spectrum of dementia, it accounts for 60-80% of all cases (Kamboh 2018, p133-135). Up to now, research has shown there are three primary risk factors for Alzheimer’s: genetics, age and cardiovascular health.
In Alzheimer’s an abnormal build-up and clumping of proteins called plaques in between neurones severs cell function and this combined with neurofibrillary tangles which disrupt the synaptic communication between neurones. Such physiological alterations, over time, cause changes in behaviour and a decline in the capacity to complete activities of daily life, ADLs (National Institute of aging, 2017). Alzheimer’s typically affects people over the ages of 65 and every five years on from this start point the risk of developing the disease doubles (Alzheimer’s Society 2019). However, there are exceptions. Symptoms of Alzheimer’s can be exhibited in adults as young as 40. This is referred to as early onset Alzheimer’s disease and is thought to be caused by mutations in genes Presenilin 1 (PSEN1), Presenilin 2 (PSEN2) and Amyloid Precursor Protein (APP), in chromosomes 1, 14 and 21 respectively (Bhushan 2018, p3).
Late onset Alzheimer’s disease (AD) can also be caused by genetic alterations and even has a greater risk in terms of polygenetic inheritance because heritability is estimated to be as high as 79% in 95% of late onset Alzheimer’s cases as demonstrated by the research of Gatz M, et al (2006, p133-135). The gene responsible is apolipoprotein E (APOE) which exists as three variants (APOE 2,3 and 4) and found in chromosome 19 (Zhang et al. 2006, p168-174). Each human inherits two of these genes (one from each parent), but is the combination of these which determines the risk of disease. Research suggests there are other genes which are risk factors associated with fat metabolism, inflammation and cellular transport such as MS4A, CD33, PICALM, BIN1, ABCA7, CLU, CR1, EPHA1 and CD2AP. However, the risk is lesser than that of APOE variants. Genetics alone doesn’t cause Alzheimer’s, instead it is a combination of other factors: age and cardiovascular health (Alzheimer’s Society 2019).
Cardiovascular disease (CVD) is the umbrella term for disorders in the heart, circulatory system and blood vessels (Felman 2018). Antecedent risk factors including hypertension (high blood pressure) (Cheng et al. 2011, p424-430) smoking and lipid disorders increase the risk of developing AD (Tosto et al 2016, p1231-1237). CVD has been shown to affect dementia by reducing cerebral blood flow which causes poorer cognitive performance (Bangen et al. year?). Additionally, it is thought to decompose the blood-brain barrier which is important as its purpose is to protect the brain from changes in plasma compositions (Abbott N.J. 2002 p629-638). Interestingly, a study conducted by the Jama Neurology Network suggested that hypertension could possibly protect against AD and lower its risk. However, it could also lead to stroke which in turn increases the risk of AD greatly. This is because stroke is predisposing with a diagnosis of Alzheimer’s if in combination with other CVD diseases.
Symptoms of Alzheimer’s are categorised in stages, ranging from mild to moderate and moderate to severe. The National Institute on Ageing (year?) states that mild symptoms encompass: memory loss, lack of initiative, taking longer to complete ADLs, asking repetitive questions, getting lost and losing personal belongings. They also appear to have an increase in aggressive behaviour and anxiety. It is usually at this stage that the disease is diagnosed. Bature et al. (2017) discovered that in all cases of people with late-onset AD 98.5% suffered from the primary symptoms of depression and 99.1% suffered from cognitive impairment as primary symptoms, respectively. Memory loss typically begins 12 years before official clinical diagnosis and worsens to the extent of losing all motor skills but this is in the very last stage of Alzheimer’s disease.
AD is diagnosed through numerous methods, such as biomarkers, memory tests and changes in behaviour. The disease is generally hard to detect and goes unnoticed in the beginning as behavioural and memory changes are generally unreported and instead concluded as being coincidence. In addition, it cannot be definitely identified by one singular physical scan, or examination. In fact, for a definite diagnosis, autopsy confirmation is required which means the patient has already become deceased (Shaw et al. 2009, p403-413). The current methods of identification are cerebrospinal biomarkers, such as; phospho-tau, total-tau and beta amyloid in the 42 amino acid form. These differentiate and determine different neurological diseases. Another diagnostic is the use of vector machines to differentiate AD from frontal-temporal lobar degeneration and normal aging which has a 95% accuracy level (Brain, 2008 p2969-2974).
The cure for Alzheimer’s disease is currently non-existent. Instead current medical research just allow for the management of the disease to maintain the well-being and functionality of the patient as an individual for as long as possible. Such medications include cholinesterase inhibitors and memantine which help to recuperate memory and attentiveness. Alternatively, natural treatments would include making modifications to diet and lifestyle to reduce cardiovascular risks and in turn reduce Alzheimer risks: Weller and Budson (2018) found that it is possible to prevent overall cognitive atrophy by just improving the patient’s lifestyle. In fact, this is the first thing diagnosed patients are recommended to change regardless of their stage in AD (Weller J. and Budson A. 2018).
The cholinesterase inhibitors utilized are donepezil, rivastigmine and galantamine which act to decrease the chemical breakdown of acetylcholine which is a chemical responsible for the transmission of signals between nerve cells. However, nerve cells are progressively lost from the use of acetylcholine because it breaks down in the brain. A decrease in acetylcholine and the worsening of AD symptoms are inextricably linked. The drugs mentioned above are called inhibitors because they inhibit the enzyme acetylcholinesterase which decomposes acetylcholine in the brain. Consequently, the transient increase of acetylcholine in the brain results in better communication between nerve cells which temporarily alleviate symptoms. On average the palliative treatment is effective for 6 to 12 months. Unfortunately, after this period, symptoms slowly worsen. The benefits of the drug outweigh the inevitable damage which proceeds it. However, there are contradictory thoughts about these drugs even though most people benefit from improved ability to complete ADLs, motivation, memory, concentration and reduced anxiety (Alzheimer’s Society 2014). Memantine is another drug used to treat AD, although unlike the other drug treatments it is usually administered to patients in the moderate to severe symptom category because of evidence suggesting it can help decrease delusions, agitation and aggression as recommended by The NICE guidance (2011). Memantine functions by blocking the brain from exposure of excess glutamate, a chemical which in excess causes damage to brain cells but otherwise transduces signals to and from nerve cells). Unfortunately, glutamate is released excessively after brain cells are damaged by AD creating a cycle of damage (Alzheimer’s Society 2014).
The research can suggest that the battle against Alzheimer’s disease is far from over. Drugs without side effects and with higher effectiveness need to be created. Presumably, the next steps to tackling the disease involves a method to detect the beginning of the formation of tau tangles and tangles in the neurofibrils, after all it is these factors which are the start point of a plethora of symptoms: the aftermath being possible incontinence and the inability to walk, move and talk. Additionally, other drugs need to be developed because the inhibitors only provide temporary relief. AD is primarily associated with age. But questions still remain: why do humans begin a process of degeneration? why are human bodies susceptible to degenerative changes when aged over 65 years? Perhaps looking at Alzheimer’s from a different angle will lead to results and hopefully one day a real cure.
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