Cultured GABA-immunoreactive neurons are resistant to toxicity induced by beta-amyloid.
Neurodegeneration in Alzheimer's disease is characterized by a selective loss of particular cell populations. Several recent lines of evidence suggest that beta-amyloid protein directly contributes to the disease's progression and is likely responsible for the observed pattern of neuronal death. We have previously demonstrated that aggregated beta-amyloid peptides are neurotoxic to cultured neurons. We now report that a neuronal population exhibiting GABA-immunoreactivity is resistant to beta-amyloid-induced toxicity in vitro, a finding consistent with observations in the Alzheimer brain. Determination of the intrinsic neuronal characteristics responsible for resistance to beta-amyloid may prove beneficial in both understanding the mechanism(s) of beta-amyloid neurotoxicity and halting the disease's progressive neuronal degeneration.
Pike
C J
CJ
Irvine Research Unit in Brain Aging and Alzheimer's Disease, Department of Psychobiology, University of California.
Cotman
C W
CW
D000544:Alzheimer Disease / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000633:toxicity*; D015415:Biomarkers; D002478:Cells, Cultured; D004351:Drug Resistance; D009410:Nerve Degeneration; D009474:Neurons / Q000187:drug effects*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D016229:Amyloid beta-Peptides; D015415:Biomarkers; D005680:gamma-Aminobutyric Acid