Cholesterol On Alzheimer Transfer Genetic Animal Model Of App Processing And A¦Â Generated

Alzheimer's disease (AD) is a common neurodegenerative disease, which is characterized clinically by a progressive loss of memory and cognitive impairment. Its main neuropathological features include diffuse loss of neurons in the hippocampus and neocortex, neurofibrillary tangles, accumulation of extracellular amyloid or senile plaques. A main constituent of these amyloid plaques is the β- amyloid (Aβ), a 39-43-amino-acid protein derived from the processing of a large transmembrane protein, the 3 -amyloid precursor protein (APP). The amyloid hypothesis postulated that the accumulation of A 3 in the brain, resulting from abnormal processing of APP to A β or reduced clearance of A 3 from brain, is the primary cause of AD. Now many epidemiologic investigations indicate that hyperlipoidemia may relate to the pathogenesis of AD. It is recognized that high cholesterol and high fat diet is a risk factor of AD and more and more epidemiologic, in vitro and in vivo tests show that cholesterol plays an important part in the processing of APP and the biosynthesis of A β . Some experiments illuminated that cholesterol-lowing drug statin could reduce the biosynthesis of A 3 from APP in AD transgenic animal models, but some researchers considered that its protection of AD had no direct relationship with the function of lowering cholesterol.