Alzheimer Disease

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In this study we try to explore the concept of “Alzheimer Disease” in a holistic context. The main focus of the research is on “Alzheimer Disease”. The research also analyzes many aspects of “Alzheimer Disease” and tries to gauge its effect on “A Person's Health”. Finally the research describes various factors which are responsible for “Alzheimer Disease” and tries to describe the overall effect of “Alzheimer Disease”.

Table of Contents



Methods of Research on Alzheimer's4

Opinions for Future Research of Alzheimer's7


Alzheimer Disease


Alzheimer's disease (AD) is an incurable, progressive dementia characterized by cognitive deficits in language, speech, memory, and the ability to perform motor skills. It causes significant impairment in social and occupational functioning that presents serious difficulties to the patient and family members. Disease progression is variable, but AD, due to the associated neurodegenerative complications, is always fatal. Changes in brain structure and function characteristic of AD include amyloid plaques (i.e., deposits of ß-amyloid protein), neurofibrillary tangles (i.e., abnormal collections of twisted protein threads inside neurons), synapse deterioration, and brain cell death, particularly in the frontal and temporal lobes. Production of neurotransmitters (e.g., acetylcholine) is decreased. The etiology of AD is unknown, but various dysfunctions may contribute to the pathogenesis of AD; these include aberrant iron deposition, oxidative stress, mitochondrial insufficiency, calcium homeostasis, neuro-inflammatory responses, cerebrovascular ischemia, and altered glucose and insulin metabolism. In addition, mutations in genes that code for proteins have been identified as causing AD, including genes for the proteins amyloid precursor protein (APP), presenilin 1, presenilin 2, and apolipoprotein E (APOE).

There are no definitive diagnostic imaging or laboratory tests for AD; diagnosis is confirmed only upon autopsy. Clinical diagnosis is based on patient history, a thorough physical and neurologic examination, and the use of reliable and valid diagnostic criteria. AD should be differentiated from other dementias, such as Parkinson's disease, vitamin/nutritional deficiencies, Huntington's disease, Creutzfeldt-Jakob disease, brain tumors, substance abuse, and depression. Pharmacologic treatment modestly improves cognitive symptoms and may slow progression of the disease, particularly if given in early-stage AD. Therapeutic activities (e.g., memory enhancing exercises, occupational therapy), home modifications, and the use of modified communication are often useful in keeping the patient engaged and safe.


The cause for Alzheimer's is the loss of brain cells and changes in the outer layer of the brain or the cerebral cortex. Plaques and/or tangled fibers form around the nerve cells in the cerebral cortex. Plaques are protein deposits that build up between the nerve cells while tangles form inside the dying nerve cells. In a healthy brain, nerve cells pass information to each others by using chemicals. Two of these chemicals are acetylcholine and acetyl cholinesterase. Acetylcholine helps pass signals between the nerve cells in the brain. Acetyl cholinesterase controls the flow of signals by breaking down acetylcholine. As the disease, progresses, the nerve cells are lost, and the flow of chemical signals slows down. As these nerve cells are lost there, is less acetylcholine to carry the signals. The acetyl cholinesterase is working as usual, which means fewer signals ...
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