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Modulating adult neurogenesis affects synaptic plasticity and cognitive functions in mouse models of Alzheimer's disease.

ABSTRACT: New neurons are abnormal in the adult hippocampus of Alzheimer's disease (AD) mouse models. The effects of modulating adult neurogenesis on AD pathogenesis differ from study to study. We reported recently that ablation of adult neural stem cells (aNSCs) was associated with improved memory in AD models. Here, we found that long-term potentiation (LTP) was improved in the hippocampus of APP/PS1 mice after ablation of aNSCs. This effect was confirmed in hAPP-J20 mice, a second AD mouse model. On the other hand, we found that exposure to enriched environment (EE) dramatically increased the number of DCX⁺ neurons, promoted dendritic growth, and affected the location of newborn neurons in the dentate gyrus of APP/PS1 mice, and EE exposure significantly ameliorated memory deficits in APP/PS1 mice. Together, our data suggest that both inhibiting abnormal adult neurogenesis and enhancing healthy adult neurogenesis could be beneficial for AD, and they are not mutually exclusive.

SUBMITTER: Zhang X

PROVIDER: S-EPMC8693766 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature

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Modulating adult neurogenesis affects synaptic plasticity and cognitive functions in mouse models of Alzheimer's disease.

Zhang Xiaoqin X Wei Xiaojie X Mei Yufei Y Wang Dongpi D Wang Jing J Zhang Yiping Y Li Xuekun X Gu Yan Y Peng Guoping G Sun Binggui B

Stem cell reports 20211202 12

New neurons are abnormal in the adult hippocampus of Alzheimer's disease (AD) mouse models. The effects of modulating adult neurogenesis on AD pathogenesis differ from study to study. We reported recently that ablation of adult neural stem cells (aNSCs) was associated with improved memory in AD models. Here, we found that long-term potentiation (LTP) was improved in the hippocampus of APP/PS1 mice after ablation of aNSCs. This effect was confirmed in hAPP-J20 mice, a second AD mouse model. On th ...[more]

PMID: 34861165

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Project description:IntroductionCognitive decline is a central manifestation of Alzheimer's disease (AD), and its process is inseparable from changes in synaptic plasticity. The aim of this review was to summarize and evaluate the effectiveness of exercise on cognitive function and synaptic plasticity in AD animal models.Materials and methodsEligible studies were searched from PubMed, MEDLINE, EMBASE, Web of Science, and Cochrane Library from April to May 2022. The risk of bias was evaluated by Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE). The Morris water maze (MWM) test and synaptic plasticity were considered outcome measures. Data were analyzed using random-effects meta-analyses using the software Stata. Heterogeneity was examined by using I2 test. Sensitivity analysis and publication bias were also assessed.ResultsA total of 20 randomized controlled studies were eligible for study inclusion. Compared with controls, exercise decreased escape latency (SMD = -0.86, 95% CI: -1.21 to -0.50, P < 0.001), increased platform crossover numbers (SMD = 1.34, 95% CI: 0.57-2.11, P = 0.001) and time in the target quadrant (SMD = 1.65, 95% CI: 0.95-2.36, P < 0.001) and the expression of PSD95 (SMD = 0.73, 95% CI: 0.25-1.21, P = 0.003) in AD animals. The results of the subgroup analysis showed that exercise before AD had a greater effect on escape latency (SMD = -0.88, 95% CI: -1.25 to -0.52, P < 0.001), platform crossover numbers (SMD = 1.71, 95% CI: 1.23-2.18, P < 0.001), time in the target quadrant (SMD = 2.03, 95% CI: 1.19-2.87, P < 0.001) and the expression of PSD95 (SMD = 0.94, 95% CI: 0.19-1.69, P = 0.014) than exercise after AD. The results of the subgroup analysis also showed that treadmill running might be an appropriate exercise type.ConclusionOur findings suggested that exercise had a potential effect on improving cognitive function and synaptic plasticity. It can play a better neuroprotective role before AD.Systematic review registrationPROSPERO, identifier: CRD42022328438.

Dataset Information

Modulating adult neurogenesis affects synaptic plasticity and cognitive functions in mouse models of Alzheimer's disease.

Publications

Modulating adult neurogenesis affects synaptic plasticity and cognitive functions in mouse models of Alzheimer's disease.

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