CAS BI 525 Lecture Notes - Lecture 28: Trisomy, Amyloidosis, Presenilin
17 Dec 2016
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Review: app is found of chromosome 21, tau chromosome 17, tau (phf for protofibrils and nft for fibrils) Beta amyloid: not equal to amyloid, a peptide from app, 4 kda peptide (abeta40, abeta42, beta amyloid is insoluble in water, when released form precursor protein, beta amyloid assumes a beta-sheet conformation hydrophobic (insoluble in water) Misfolding lose ability to become soluble: beta amyloid peptides form oligomers that are toxic and will aggregate into fibrils, forming the core of the beta-amyloid plaque, size of the plaque will increase as disease progresses. Cause or consequence of ad: beta amyloid pathology may influence tau pathology, even though they work via different mechanisms, when plaques form, nearb(cid:455) (cid:374)euro(cid:374)s (cid:862)(cid:271)e(cid:374)d(cid:863), whi(cid:272)h (cid:373)a(cid:455) (cid:271)e a sig(cid:374) of to(cid:454)i(cid:272)it(cid:455), (cid:271)ut (cid:374)ot necessarily neurodegeneration. Genetic ad- depending on the kind of mutation and the gene that carries it, onset is much earlier in genetic than in sporadic (<65 years: all mutations are autosomal dominant and involve:
