Comparing Alzheimer’s Disease and Parkinson’s Disease

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There are many superficial similarities between Alzheimer’s disease and Parkinson’s disease primarily in some symptoms and age-group of persons afflicted by these two diseases. Nonetheless, these two are inherently distinct and distinguishable from each other in many aspects such as etiology and treatment, for example.

Alzheimer’s disease is a progressive and lethal neurodegenerative disorder characterized by cognitive and memory decline (Cummings, 2004). Due to this performance of daily activities are severely affected. In addition, a range of neuropsychiatric and behavioral symptoms are also observed. The prevalence of the disease is notable since in the United States alone there are approximately 4.5 million sufferers in 2000 (Hebert et al., 2003).

Parkinson’s disease is likewise a neurodegenerative disorder manifested by motor function symptoms such as tremor and rigidity accompanied by dementia in advanced cases although there are nine differential diagnoses of Parkinsonism (Rao et al., 2006). The prevalence of Parkinson’s disease in the US population is pegged at 0.3 percent (de Lau, 2004) and one million in United States alone (Zigmond & Burke, 2002).

This paper aims to identify the characteristics of Alzheimer’s and Parkinson’s diseases including their etiology, pathology and pathophysiology, clinical presentations, natural history and prognosis, diagnosis, treatment and other current and relevant information with the purpose of establishing the similarities and differences between the two diseases.

Regarding etiology, Alzheimer’s and Parkinson’s diseases share common characteristics since both are induced at some level by genetic conditions. Alzheimer’s disease has a complex hereditary relationship. In 20 percent of early-onset cases of Alzheimer’s disease, it is found to be inherited in autosomal manner although in late-onset cases genetic factors are said to play a role in the incidence of familial aggregation. There are three genes identified to be responsible in early-onset Alzheimer’s disease; these are APP, presenilin 1 and presenelin 2 which are inherited in autosomal dominant manner (Brice, 2004). APP is located in chromosome 21 while presenelin 1 is involved in point mutations while presenelin 2 are not associated with such genetic aberrations. In late-onset cases of Alzheimer’s disease the gene ApoE is implicated as a risk factor (Brice, 2004).

Parkinson’s disease, on the other hand, is also considered to be brought about by the interaction between various genes and environmental factors which are currently not yet fully researched. Nonetheless, there are several loci being studied for their association with familial parkinsonism which are PARK1-PARK11. Four of seven genes from these loci were found to cause autosomal dominant -synuclein. The other three, parkinsonism; these are LRRK2, UCHL1, NURR1, and namely DJ1, PINK1 and parkin, were identified as inducing autosomal recessive disorder (Tolosa et al., 2006).

In terms of pathology and pathophysiology, Alzheimer’s and Parkinson’s disease largely differ. Alzheimer’s disorder experts point to the generation and increase of beta-amyloid peptide as the pathological characteristics of the disease according to Cummings (2004). This is supported by the observation of amyloid precursor protein mutations in cases of late-onset Alzheimer’s disease and the increase in the production of beta-amyloid peptide are invariably traced back in all mutations associated with Alzheimer’s disease (Hardy & Selkoe, 2002).

On the other hand, Parkinson’s disease is characterized by loss of DA or dopamine neurons which are located in the substantia nigra pars compacta (SNpc) according to Zigmond & Burke (2002). The authors added that up to 60 percent of DA neurons are lost even in mild Parkinson’s disease patients while remaining neurons may become dysfunctional which result to the 80 percent total loss of DA neurons in the corpus striatum. Another pathological sign of this disease is the Lewy body which is an eosinophilic inclusion located inside neurons which are associated with brain regions showing severe neuron loss (Zigmond & Burke, 2002).

For clinical presentations, a range of symptoms are involved in both Alzheimer’s and Parkinson’s. While the primary clinical presentations of Alzheimer’s are cognitive or mental dysfunction, Parkinson’s is characterized more of motor function abnormalities. Alzheimer’s disease is commonly associated with recent memory loss, aphasia and apraxia. Advance cases manifest psychiatric or behavioral abnormalities, extrapyramidal syndrome, epileptic attacks and myoclonia (Brice, 2004). Cummings (2004) put the classical features of Alzheimer’s memory impairment of amnesic kind, language decline and visuospatial problems with accompanying motor and sensory disorders such as walking problems and seizures.

On the other hand, Parkinson’s disease is characterized by shaking or trembling, stiffness and slowness of movements. In addition to these motor function aberrations are mental or cognitive features such as dementia or dysautonomia. Forty percent of Parkinson’s disease patients may suffer depression. Furthermore, around half of patients experience pain and sensory symptoms secondary to the degree of motor impairment mentioned above. However, nine differential diagnoses is present in Parkinson’s disease with different sets of signs and symptoms. For example, idiopathic Parkinson’s disease presents with tremor, bradykinesia, rigidity, poor gait and micrographia while vascular parkinsonism can be characterized by fixed discrepancies from previous events, and dementia with Lewy bodies diagnosis can be manifested by impaired attention and syncope among other persistent symptoms (Rao et al., 2006).

In terms of natural history and prognosis, Parkinson’s disease provides a wider range of characteristics compared to Alzheimer’s which is due to the various differential diagnoses that are available to the latter. For instance, idiopathic Parkinson’s disease includes historical features such as difficulty with activities, stiffness and tremor. Drug-induced parkinsonism involves previous use of a causative chemical while normal-pressure hydrocephalus requires ataxia, urinary incontinence and dementia. On the other hand, Alzheimer’s disease has limited natural history characteristics that are indicative of the disease. Nonetheless, problems in global cognitive ability and episodic memory are somewhat implied according to Backman et al. (2005).

Regarding diagnosis, Parkinson’s understandably involves various symptoms and characteristics for the establishment of diagnoses included in the disease spectrum while Alzheimer’s does not necessitate as much such that different tests are required for the former compared to the latter. In Parkinson’s disease a series of tests are needed to determine if the presented case is idiopathic Parkinson’s disease, drug-induced parkinsonism, vascular parkinsonism or any of the other six diagnoses. In order to establish such diagnoses, genetic testing may be used to evaluate the seven genes located in the PARK loci described above. Drug challenge more specifically dopaminergenic responsiveness, neurophysiology detailing relevant brain motor functions, autonomic function testing such as cardiovascular, olfactory test for hyposmia, computed tomography and magnetic resonance imaging are all very useful tools for the diagnosis of Parkinson’s disease (Tolosa, 2006).

On the other hand, the classic features or symptoms described above are initially used for Alzheimer’s disease diagnosis. Next to this is the assessment of psychological or behavioral disturbances that the patient may present such as performance of daily activities, mood swing, apathy, psychosis and agitation. Laboratory tests for the determination of dementia include thyroid-function tests, serum electrolyte, blood glucose, serum vitamin B12 measurement, blood count, blood urea nitrogen measurement and liver-function tests (Cummings, 2004). In addition to these, other specialized laboratory tests for syphilis, erythrocyte and human immunodeficiency virus are also necessary to establish dementia. Computed tomography and magnetic resonance imaging can be used to diagnose Alzheimer’s disease while positron-emission tomography and single-photon-emission computed tomography are used for differential diagnosis dementia-related diseases.

In terms of treatment, understandably Parkinson’s disease and Alzheimer’s disease require their own set of chemical and other forms of intervention. Both treatment regimens include circumventing the biochemical processes involved in the induction of the disease while others relieve or suppress some of the pain or symptoms. For Alzheimer’s disease the use of antioxidants such as vitamin E or alpha-tocopherol (Sano et al., 1997); an N-methyl-D-aspartate antagonist called memantine(Danysz & Parsons, 2003); cholinesterase inhibitors such as tacrine, rivastigmine, donepezil and galantamine are being both recommended and evaluated at the present (Watkins et al., 1994).

On the other hand, medications for Parkinson’s disease that are FDA-approved include anticholinergics such as benztropine and trihexyphenidyl, carbidopa or levodopa, COMT inhibitors such as entacapone and tolcapone, dopamine agonists such as bromocriptine and pergolide, MAO-B inhibitors such as selegiline and rasagaline, and NMDA receptor inhibitor such as amantadine (Rao et al., 2006)

Current issues that are facing the diagnosis and treatment of Parkinson’s disease include the low level of diagnosis certainty necessitating newer technology, exploring nonpharmacologic treatment strategies and cost-effectiveness of recommended procedures (Delagarza, 2003). According to Tolosa (2006), the clinical diagnostic uncertainty for Alzheimer’s disease is high at the early stage of presentation. This fact results to reclassification of 30 percent of patients initially diagnosed with the disease (Tolosa, 2006). According to Rao et al. (2006), nonpharmacologic interventions may not be the magic bullet for Parkinson’s but can be helpful in sustaining the patient’s welfare. Cost-effectiveness of modern diagnostic methods based on computed tomography and magnetic resonance imaging are not yet established (Tolosa, 2006).

On the other hand, the elucidation of preclinical characteristics of Alzheimer’s disease, concerns on fatal cases with emphasis on health maintenance and treatment of related complications, and the importance of the role of caregivers for the welfare of affected persons (Cummings, 2004). Cummings adds that septicemia, pneumonia and other diseases may lead to death in Alzheimer’s cases necessitating development of better health maintenance. According to Backman et al. (2005), there is a need to combine predictors of Alzheimer’s disease from multiple behavior and biological aspects for the improvement of diagnosis involving preclinical characteristics.

In conclusion, upon identification of the different characteristics of Alzheimer’s and Parkinson’s disease regarding etiology, pathology and pathophysiology, clinical presentations, natural history and prognosis, diagnosis, treatment and other current issues, the unique features of each disorder were obtained. Although both are neurodegenerative diseases and afflict the same age group, the etiology, pathophysiology, diagnosis and treatment are inherently divergent including the current issues besetting the strategies for their management.

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Comparing Alzheimer’s Disease and Parkinson’s Disease

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