الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Alzheimer’s Disease is a protein misfolding disease due to accumulation of amyloid beta and tau forming neuritic plaques and neurofibrillary tangles causing death of neurons. AD can be classified into sporadic and familial types. Sporadic type represents 75% while familial type have 4 types:1,3 and 4 (early-onset) and type 2 (late-onset). Three genes have been identified to cause early-onset AD: Amyloid precursor protein, presenilin 1 and 2. Apolipoprotein E and Sortilin-related receptor 1 have been associated with late-onset AD. The incidence of AD is increased following cerebral ischemia and strokes in which hypoxia occurs in affected brain areas. Overexpression of hypoxia-inducible factor 1 increases beta secretase activity which increases amyloid beta production. Atherosclerosis is important in pathogenesis of AD. There is a biochemical and genetic relationship between cholesterol and AD including polymorphisms of ATP binding cassette transporter A1, Apolipoprotein E and cholesterol 24- hydroxylase.