Sandbox Reserved 595: Difference between revisions
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=Clinical Relevance= | =Clinical Relevance= | ||
==Late Onset Alzheimer's Disease== | |||
Inheritance of the ε4 allele is considered to be the strongest genetic risk factor for late onset Alzheimer's disease (LOAD) (A). Late onset Alzheimer's disease is characterized by the presence of plaques. Amyloid-β, a hydrophobic peptide, is a major component of these plaques (T). ApoE has been observed to tightly bind with Aβ, an interaction that is hypothesized to influence the deposition of Aβ, thus contributing to the pathogenesis of LOAD (F). A significant amount of Aβ is concentrated within the small paopulation of apoE-containing synapses; these two molecules have been observed to be highly colocalized in these synapses (R). Concentrations of amyloid-β in the extracellular space of the brain are indicative of the balance between the synthesis and clearance of Aβ (S). In fact, the Aβ concentration per synaptic terminal is notably lower in control subjects as compared to those exhibiting AD (R). A deficit in clearance, rather than aberrant synthesis, is thought to be a factor in plaque formation (R). | |||
=References= | =References= | ||
