Amyloid 17-42

Amyloid 17-42 (Aβ(17-42)) is a major constituent of diffuse plaques in Alzheimer's disease and cerebellar pre-amyloid in Down's syndrome, derived by alpha- and gamma-secretase cleavage of the amyloid precursor protein (APP). Amyloid 17-42 can induce neuronal Apoptosis via a Fas-like/caspase-8 activation pathway[1].

Signaling Pathways >> Apoptosis >> Apoptosis

Research Areas >> Neurological Disease

Amyloid 17-42 (20 μM; 48 h) leads to apoptosis in SH-SY5Y and IMR-32 cells[1]. Amyloid 17-42 (20 μM; 48 h, 72 h) activates caspase-8 and caspase-3, induced poly(ADP-ribose) polymerase cleavage[1]. Amyloid 17-42 (20 μM) moderately activates c-Jun N-terminal kinase (JNK)[1]. Amyloid 17-42 induces neuronal apoptosis via a Fas-like/caspase-8 activation pathway[1]. Cell Cytotoxicity Assay[1] Cell Line: SH-SY5Y and IMR-32 cells Concentration: 0-30 μM Incubation Time: 48 h Result: Caused the death of SH-SY5Y and IMR-32 human neuroblastoma cells. Apoptosis Analysis[1] Cell Line: SH-SY5Y cells Concentration: 20 μM Incubation Time: 48 h Result: Showed shrunken cell bodies, condensed and fragmented chromatin, and increased amounts of cytoplasmic oligonucleosomes. Western Blot Analysis[1] Cell Line: SH-SY5Y cells Concentration: 20 μM Incubation Time: 48, 72 h; 18 h, 24 h Result: Reduced procaspase-3 and increased cleaved caspase-3 in cells. Reduced procaspase-8 in cells. Lead to early activation of JNK.

[1]. Wanli Wei, et al. Abeta 17-42 in Alzheimer's disease activates JNK and caspase-8 leading to neuronal apoptosis. Brain. 2002 Sep;125(Pt 9):2036-43.