Bing Chun Yan1,2, Dan Jiang3, Jie Wang3, Yuanyuan Zhang4, Xiaolu Zhu3, Pei Xu3, Xing Yu5, Moo-Ho Won6, Pei Qing Su3. 1. Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou, 225001, People's Republic of China. bcyan@yzu.edu.cn. 2. Department of Neurology, Affiliated Hospital, Yangzhou University, Yangzhou, 225001, People's Republic of China. bcyan@yzu.edu.cn. 3. Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou, 225001, People's Republic of China. 4. Department of Neurology, Affiliated Hospital, Yangzhou University, Yangzhou, 225001, People's Republic of China. 5. Department of Pharmacy, Yangzhou Maternal and Child Care Service Center, Yangzhou, 225002, People's Republic of China. 6. Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea.
Abstract
BACKGROUND: Aging is an inevitable process which results in many changes. These changes are closely related to the hippocampus which is in charge of long-term learning and episodic memory. AIM: This study was to investigate age-related changes of the cell proliferation, neuroblast differentiation and Akt/mTOR signaling in the hippocampal alveus of aged mice. METHODS: In the present study, we compared the differences of neurogenesis in the hippocampal alveus between adult (postnatal month 6) and aged (postnatal month 24) mice using immunohistochemistry and western blot analysis. RESULTS: The cell proliferation, neuroblast differentiation, and the increased astrocyte activation in the hippocampal alveus of mice were decreased in an age-dependent manner. In addition, during normal aging, the protein level of AKT, mTOR and the phosphorylation of mTOR were all decreased. However, the protein level of AKT was increased. DISCUSSION: These results indicate the neurogenesis in the immature neurons in the hippocampal alveus of aged mice was closely related to the normal aging process. In addition, during normal aging, the increased AKT phosphorylation and decreased mTOR phosphorylation in the hippocampus may play a role in aging development. CONCLUSION: The result indicates that increased activation of astrocyte, increased phosphorylation of AKT and decreased phosphorylation of mTOR may be involved in the decreased cell proliferation and neuroblast differentiation in the alveus of hippocampus of aged mice.
BACKGROUND: Aging is an inevitable process which results in many changes. These changes are closely related to the hippocampus which is in charge of long-term learning and episodic memory. AIM: This study was to investigate age-related changes of the cell proliferation, neuroblast differentiation and Akt/mTOR signaling in the hippocampal alveus of aged mice. METHODS: In the present study, we compared the differences of neurogenesis in the hippocampal alveus between adult (postnatal month 6) and aged (postnatal month 24) mice using immunohistochemistry and western blot analysis. RESULTS: The cell proliferation, neuroblast differentiation, and the increased astrocyte activation in the hippocampal alveus of mice were decreased in an age-dependent manner. In addition, during normal aging, the protein level of AKT, mTOR and the phosphorylation of mTOR were all decreased. However, the protein level of AKT was increased. DISCUSSION: These results indicate the neurogenesis in the immature neurons in the hippocampal alveus of aged mice was closely related to the normal aging process. In addition, during normal aging, the increased AKT phosphorylation and decreased mTOR phosphorylation in the hippocampus may play a role in aging development. CONCLUSION: The result indicates that increased activation of astrocyte, increased phosphorylation of AKT and decreased phosphorylation of mTOR may be involved in the decreased cell proliferation and neuroblast differentiation in the alveus of hippocampus of aged mice.
Entities:
Keywords:
Akt/mTOR signaling; Alveus of hippocampus; Cell proliferation; Neuroblast differentiation; Normal aging