Aluminum-induced amyloidogenesis and impairment in the clearance of amyloid peptides from the central nervous system in Alzheimer's disease.

摘要: The membrane-integral beta-amyloid pre-cursor protein (bAPP) is probably the mostintensively studied brain cell inneurobiology. bAPP processed by tan-dem beta-gamma secretase cleavage into42 amino acid amyloid (Ab42) peptides,whose progressive accumulation onedistinguishing feature of Alzheimer’s dis-ease (AD) neuropathology (1–3). WhilehomeostaticamountsofAb42peptidegen-eration and clearance seem to be toler-ated cells, their over-abundance,aggregation into higher order structures,and inability cells effec-tively phagocytose clear these intenselyhydrophobic peptides contribute thepro-inflammatory neurotoxic pathol-ogy AD. Aluminum, as an extremelyhigh charge density cation (