Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
328945 | Neurobiology of Aging | 2006 | 10 Pages |
Abstract
Expression of Caspase and Bcl-2 proteins was examined in the hippocampus of senescence-accelerated mice (SAM, P8 and R1 strain) from E19 to 16 months of age. Immunoblotting analysis showed no upregulation of pro-apoptotic proteins (caspase-2L, -3, -6, -8, -9, and Bax) with age while all the anti-apoptotic proteins (caspase-2S, Bcl-2, and Bcl-XL) remained unchanged during aging. Terminal dUTP nick end labeling (TUNEL) and electron microscopy on the hippocampus of 3- and 16-month-old SAM revealed very few TUNEL positive cells in both groups. Morphometric study further showed neuronal loss in the hippocampus was not age-related. Our results suggest apoptosis and cell loss are minor events in the hippocampus of SAM mice and are unlikely to be the cause of functional decline during aging in SAM.
Keywords
DABSLMSDSTerminal dUTP nick end labelingstratum oriensDTTSAMHRPstratum radiatumSAMRstratum pyramidaleTemmitphosphate bufferTUNELBcl-2 familyApoptosisGolgi apparatusCNSdithiothreitolAgingsodium dodecyl sulphatesAMPcentral nervous systemStratum lacunosum-moleculareSenescence-accelerated mouseMitochondriaTransmission electron microscopyNucleusHorseradish peroxidaseCaspasesLipofuscin granulesnuc
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Authors
Yan Wu, Ai-Qun Zhang, Maria S.M. Wai, Helen W.L. Lai, Sheng-Xi Wu, David T. Yew,