Sandbox Reserved 595: Difference between revisions
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=Clinical Relevance= | =Clinical Relevance= | ||
==Late Onset Alzheimer's Disease== | ==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). | 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). | ||
==Type III Hyperlipoproteinemia== | |||
Familial Type III hyperlipoproteinemia is a genetic lipid disorder that is marked by an increase in the concentrations of plasma cholesterol and triglyceride levels (Rall 82). Normally, in individuals whose apoE is functional, chylomicron remnants and VLDL remnants are rapidly removed from circulation via recptor-mediated endocytosis within the liver. However, this condition develops as a result of apoE that has impaired clearance abilities. When a defect in apoE of this nature is present, delayed clearance in the plasma of triglyceride-rich lipoprotein remants results; significantly elevated levels of cholesterol-encriched remnant lipoproteins are a defining feature of this disorder (W; Kashyap). Individuals homozygous for the ε2 allele are most susceptible. The E2 isoform of apoE exhibits weak or defective binding of remnants to hepatic lipoprotein receptors; the E2 isoform also clears these remnants from the plasma in a sluggish fashion (W). | |||
=References= | =References= | ||
