Up-regulation of Bcl-2 is associated with neuronal DNA damage in Alzheimer's disease.
Cell death and neurofibrillary tangle formation are prominent features of Alzheimer's disease (AD). It has been suggested that DNA damage may reflect neuronal vulnerability. In this context, the Ced homologue Bcl-2 is able to repress a number of cell death programs. Recently we found both numerous nuclei exhibiting DNA damage within neurons in the AD brain and increases in Bcl-2 immunoreactivity. In this study, we examined the relationship between Bcl-2 expression and nuclear DNA damage or tangle formation. Nuclei exhibiting DNA damage were associated with an up-regulation of Bcl-2 expression, whereas tangle-bearing neurons were associated with a down-regulation of Bcl-2 expression.
Su
J H
JH
Institute for Brain Aging and Dementia, University of California at Irvine 92717-4550, USA.
Satou
T
T
Anderson
A J
AJ
Cotman
C W
CW
D000368:Aged; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology*; D002467:Cell Nucleus / Q000378:metabolism / Q000648:ultrastructure; D004249:DNA Damage / Q000502:physiology*; D015536:Down-Regulation / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D016874:Neurofibrillary Tangles / Q000473:pathology; D009474:Neurons / Q000378:metabolism*; D010766:Phosphorylation; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis*; D015854:Up-Regulation / Q000502:physiology*; D016875:tau Proteins / Q000378:metabolism
D019253:Proto-Oncogene Proteins c-bcl-2; D016875:tau Proteins