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Alzheimer's Disease

The presence of amyloid beta protein deposits in neuronal extracellular space is one of the hallmarks of Alzheimer’s disease. The role of ApoER2 in Alzheimer’s Disease is relevant, yet incompletely understood. New evidence suggests ApoeR2 plays a major role in the regulation of amyloid beta (Aβ) formation in the brain. The Aβ peptide is derived from the cleavage of amyloid precursor protein (APP) by γ-secretase:γ-secretase:. ApoeR2 works to reduce APP trafficking by altering break down. This interaction decreases APP endocytosis leading to an increase in amyloid-β production. In addition, the expression of ApoER2 within intracellular compartments leads to increased y-secretase activity, a protease which works to cleave APP into Aβ. ^[1]

^ Herz, Joachim (June 2009). "Apolipoprotein E Receptors in the Brain". Current Opinion in Lipidology. 20 (3): 190–196. doi:10.1097/MOL.0b013e32832d3a10. PMC 2848396. PMID 19433918.{{cite journal}}: CS1 maint: date and year (link)

[1] Herz, Joachim (June 2009). "Apolipoprotein E Receptors in the Brain". Current Opinion in Lipidology. 20 (3): 190–196. doi:10.1097/MOL.0b013e32832d3a10. PMC 2848396. PMID 19433918.{{cite journal}}: CS1 maint: date and year (link)

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