APP processing in Alzheimer's disease
- 生物医学－已发表论文 
An important pathological feature of Alzheimer's disease (AD) is the presence of extracellular senile plaques in the brain. Senile plaques are composed of aggregations of small peptides called beta-amyloid (A beta). Multiple lines of evidence demonstrate that overproduction/aggregation of A beta in the brain is a primary cause of AD and inhibition of A beta generation has become a hot topic in AD research. A beta is generated from beta-amyloid precursor protein (APP) through sequential cleavages first by beta-secretase and then by gamma-secretase complex. Alternatively, APP can be cleaved by alpha-secretase within the A beta domain to release soluble APP alpha and preclude A beta generation. Cleavage of APP by caspases may also contribute to AD pathologies. Therefore, understanding the metabolism/processing of APP is crucial for AD therapeutics. Here we review current knowledge of APP processing regulation as well as the patho/physiological functions of APP and its metabolites.