Hypothesis For Alzheimer's Disease

Overview:

This paper will assess numerous neurotransmitters and pathophysiological processes that are characteristic to Alzheimer’s disease. The physical changes in brain structure, the process towards neurodegeneration, and the numerous hypotheses that are present will also be discussed. These hypotheses include the Amyloid Beta Hypothesis, the Cholinergic hypothesis, the glutamatergic/excitotoxicity hypothesis, the oxidative stress hypothesis, and the chronic inflammation hypothesis will be discussed and analyzed. These hypotheses will not be discussed as a treatment method but rather on the basis of the cellular and molecular ways in which they have an effect on Alzheimer’s disease progression. This paper is also going to examine the

Shaw, 2001). Phenserine, a novel acetylcholinesterase inhibitor, has been shown to dramatically improve cognitive performance in rodents and is currently in clinical trials (N. Greig, Brossi, 1996). Studies of rats with forebrain cholinergic abrasions, known to increase Aβ in cerebral areas of the brain, have shown that Phenserine can protect against this and reduce βAPP production in animals (Haroutunian, 1997). Moreover, the absence of inhibitors of acetylcholinesterase displays a wide range of behavioral deficits in Caenorhabditis elegans (C. elegans), ranging from mild incoordination to almost complete paralysis, when mutated (Nguyen,

Myriads of studies, such as ones conducted utilizing magnetic resonance imaging, propose that neuronal loss (measured by degeneration in select regions of the brain) may start years before symptoms of memory loss become evident (Fox NC, Crum WR 2001, Kaye JA 1997). As the brain continues to degenerate, cerebrospinal fluid fills in the space previously occupied by brain tissue. When disease progression reaches minor to moderate AD, patients undergo a decline in the aptitude to process complex thoughts (e.g. experiencing predicaments cooking a meal or balancing the checkbook), more prominent memory loss (e.g. misunderstandings regarding familiar places and trouble recalling otherwise well-known names), as well as personality and mood changes. Anatomically, atrophy spreads to additional areas of the cerebral cortex (Figure 3) (Alzheimer’s