Changes of autologous neural stem cells in the hippocampi of aging mice.
Although there is possibility of cognitive disturbance in aging people, many of them live for long life and enjoy well-functioning brain during the whole life-span. The biological basis of longevity is unknown. In this study, we investigated the influence of aging on hippocampal neural stem cells (NSCs), and the correlations between hippocampal neurogenesis and cognitive function. The result showed that the protein production and mRNA expression of nestin, and the number of BrdU(+) cells in dentate gyrus (DG) of the aged non-dementia mice were clearly higher than that in the aged dementia mice and the young adult mice. We also found that the number of NeuN(+) (neuron-specific nuclear antigen) cells in DG and CA1, choline O-acetyltransferase (ChAT, EC 2.3.1.6) production and mRNA expression in hippocampi of the aged-dementia mice were significantly reduced as compared to that of the young adult mice and the aged non-dementia mice, whereas the number of NeuN(+) cells, ChAT production and mRNA expression of the aged non-dementia mice has no difference with that of the young adult mice. Glial fibrillary acidic protein (GFAP) expression in the hippocampi of aged dementia mice significantly higher than that of the young adult mice and the aged non-dementia mice. Our results suggest that aging sometimes does not cause changing of the number of neurons and the hippocampal neurogenesis. Increment of DNA replication and neuron replacement, promotion of differentiation of neural stem cells, enhancement of neuronal proliferation, facilitation of synaptic plasticity of neurons may all benefit to the maintenance of the normal cognitive ability in the aged mice.
Li
Xu Ling
XL
Department of Neurology, the Fourth Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Wang
De Sheng
de S
Qu
Heng Yan
HY
Zhao
Bao Quan
BQ
Zhang
Ting
T
Zhou
Jian Ping
JP
Li
Qian
Q
Sun
Man Ji
MJ
D000375:Aging / Q000473:pathology* / Q000523:psychology; D000818:Animals; D002452:Cell Count; D002795:Choline O-Acetyltransferase / Q000096:biosynthesis / Q000235:genetics; D003071:Cognition; D004268:DNA-Binding Proteins; D003704:Dementia / Q000473:pathology / Q000523:psychology; D005260:Female; D005904:Glial Fibrillary Acidic Protein; D006624:Hippocampus / Q000473:pathology*; D007150:Immunohistochemistry; D007381:Intermediate Filament Proteins / Q000096:biosynthesis / Q000235:genetics; D018782:Maze Learning; D051379:Mice; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D064231:Nestin; D055495:Neurogenesis; D009474:Neurons / Q000473:pathology / Q000502:physiology*; D009687:Nuclear Proteins / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D011930:Reaction Time; D013234:Stem Cells / Q000473:pathology / Q000502:physiology*
D004268:DNA-Binding Proteins; D005904:Glial Fibrillary Acidic Protein; D007381:Intermediate Filament Proteins; D009419:Nerve Tissue Proteins; C577485:Nes protein, mouse; D064231:Nestin; C492380:NeuN protein, mouse; D009687:Nuclear Proteins; D012333:RNA, Messenger; C528900:glial fibrillary astrocytic protein, mouse; D002795:Choline O-Acetyltransferase