Three Hallmarks Of Alzheimer's Disease

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Alzheimer 's Disease
Alzheimer’s disease is not a new disease. “Alzheimer’s” was first described by German psychiatrist and neuropathologist Alois Alzheimer in 1906. Alzheimer’s disease is an irreversible, progressive disorder involving neural degeneration in the cortex that slowly destroys the memory and thinking skills, and eventually the ability to carry out activities of daily living (Karch, 2013). In most people with Alzheimer’s, symptoms first appear in their mid-60, and accounts for 60% to 80% of all cases of dementia. The prevention of Alzheimer’s disease (AD) has become a real challenge due to its rising prevalence and the lack of an effective care (Otaegui-Arrazola, Amiano, Elbusto, Urdaneta, & Martinez-Lage, 2014). This disorder
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The three hallmarks of Alzheimer’s disease are the presence of neuritic (senile) plaques, neurofibrillary tangles, and amyloid angiopathy (Grossman & Porth, 2014). The neuritic plaques are patches or flat areas composed of clusters of degenerating nerve terminals arranged around a central amyloid core. The amyloid core has a dominant component called amyloid beta, a peptide derived from the proteolysis of a larger membrane-spanning amyloid precursor protein (APP). There are numerous studies that proved amyloid beta has an important role in the pathogenesis of Alzheimer’s disease (Grossman & Porth, 2014). The normal degradation of amyloid precursor protein involves cleavage in the middle of the amyloid beta domain by a proteolytic α-secretase enzyme, with the release of two soluble nonamyloidogenic pieces γ. The amyloid precursor protein can also be cleaved at either end of the amyloid beta domain, which will lead to the release of intact and highly amyloidogenic amyloid beta that accumulates in the senile plaques as amyloid fibrils. Numerous evidences suggest that cleavage by the β- and γ-secretase leads to the generation of amyloid beta peptide (Grossman & Porth, …show more content…
The diagnosis is done based on the clinical findings; however it is difficult to predict that if a person with mild impairment will progress to Alzheimer’s disease. The confirmation of the diagnosis can be done only by the microscopic examination of the tissue obtained from a cerebral biopsy or at autopsy. The diagnostic procedures for Alzheimer’s disease involve multiple steps, and a Differential Diagnosis in Alzheimer Algorithm has been developed (Grossman & Porth, 2014). The presence of dementia established by clinical examination and documented by the results of a Mini-Mental State Examination, Blessed Dementia Test, or similar mental status test; no disturbance in consciousness; onset between 40 and 90 years of age, most often after 65 years of age; and absence of systemic or brain disorders that could account for the memory or cognitive deficits all provides a baseline for the diagnosis of Alzheimer’s disease (Grossman & Porth, 2014). The presence of other brain disease is assessed by brain imaging, CT scan or MRI. Metabolic screening should be done for known reversible causes of dementia such as vitamin B12 deficiency, thyroid dysfunction, and electrolyte imbalance (Grossman & Porth, 2014). After a thorough physical examination, history collection, neurological assessments, mental status tests, and by

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