Open AccessApoptosis is induced by beta-amyloid in cultured central nervous system neurons.
Author(s) -
Deryk Loo,
Agata Copani,
Christian J. Pike,
Edward R. Whittemore,
Andrea J. Walencewicz,
Carl W. Cotman
Publication year - 1993
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.90.17.7951
Subject(s) - neurodegeneration , apoptosis , dna fragmentation , aurintricarboxylic acid , programmed cell death , biology , microbiology and biotechnology , fragmentation (computing) , amyloid beta , alzheimer's disease , chromatin , dna damage , neuroscience , dna , biochemistry , peptide , pathology , disease , medicine , ecology
The molecular mechanism responsible for the neurodegeneration in Alzheimer disease is not known; however, accumulating evidence suggests that beta-amyloid peptide (A beta P) contributes to this degeneration. We now report that synthetic A beta Ps trigger the degeneration of cultured neurons through activation of an apoptotic pathway. Neurons treated with A beta Ps exhibit morphological and biochemical characteristics of apoptosis, including membrane blebbing, compaction of nuclear chromatin, and internucleosomal DNA fragmentation. Aurintricarboxylic acid, an inhibitor of nucleases, prevents DNA fragmentation and delays cell death. Our in vitro results suggest that apoptosis may play a role in the neuronal loss associated with Alzheimer disease.