Alzheimer's Disease in the Elderly

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Walk into any senior home nowadays and there will be at least one person afflicted with Alzheimer’s disease (AD). This progressive, neurodegenerative disorder affects more than five million Americans and is projected to steadily grow in incidence every year (Alzheimer’s Association). While current research efforts have looked to determine how and why AD is caused, the pathogenesis of the disease in patients is affected by numerous factors. A variety of genetic mutations can influence the severity and time course of AD. However, researchers acknowledge that the presence of a gene and its corresponding protein does not guarantee onset (Hardy). Rather, external elements such as lifestyles, coupled with the action of multiple genes characterize AD as a complex trait. One hallmark of AD is amyloid beta plaques, large aggregates found in the patient brains composed of the peptide, amyloid beta. These amyloid plaques form the basis for the primary hypothesis behind AD, the amyloid cascade hypothesis. The cascade begins with amyloid precursor protein (APP). APP is cleaved by two different enzymes to produce one amyloid beta monomer, which aggregates with other monomers to form cytotoxic structures. These then cause the neuronal cell death and loss of synaptic function that occurs in AD (Laferla). Mutations that affect this cascade are thus of primary importance. There are three main genes, APP, PS1, and PS2, that when mutated alter the metabolism or stability of the amyloid beta

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