Alzheimer disease
Core of basic research: Focus on the formation mechanisms of Aβ amyloid deposition (senile plaques) and tau protein hyperphosphorylation (neurofibrillary tangles), explore the role of APP processing (BACE1, PS1/PS2) and tau phosphorylation-regulating enzymes (GSK3β), as well as the impact of ApoE genotype on disease risk.
Core key proteins: Aβ (β-amyloid protein forming toxic aggregates upon deposition), Tau protein (forms tangles upon hyperphosphorylation), APP (amyloid precursor protein processed to produce Aβ), PS1/PS2 (presenilins involved in APP cleavage), BACE1 (β-secretase initiating APP cleavage), IDE (insulin-degrading enzyme degrading Aβ), ApoE (affects Aβ clearance, ε4 subtype increases risk).
Core key proteins: Aβ (β-amyloid protein forming toxic aggregates upon deposition), Tau protein (forms tangles upon hyperphosphorylation), APP (amyloid precursor protein processed to produce Aβ), PS1/PS2 (presenilins involved in APP cleavage), BACE1 (β-secretase initiating APP cleavage), IDE (insulin-degrading enzyme degrading Aβ), ApoE (affects Aβ clearance, ε4 subtype increases risk).
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