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Effects of mesenchymal stem cells transplantation on cognitive deficits in animal models of Alzheimer's disease: A systematic review and meta-analysis

期刊

BRAIN AND BEHAVIOR
卷 8, 期 7, 页码 -

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WILEY
DOI: 10.1002/brb3.982

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Alzheimer's disease; animal models; cognitive deficits; mesenchymal stem cells; meta-analysis; morris water maze

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Background: Alzheimer's disease(AD) is a globally prevalent neurodegenerative disease, clinically characterized by progressive memory loss and gradual impairment of cognitive functions. Mesenchymal stem cells (MSCs) transplantation has been considered a possible therapeutic method for Alzheimer's disease (AD). However, no quantitative data synthesis of MSC therapy for AD exists. We conducted asystematic review and meta-analysis to study the effects of MSCs on cognitive deficits in animal models of AD. Methods: We identified eligible studies published from January 1980 to January 2017 by searching four electronic databases (PubMed, MEDLINE, EMBASE, CNKI). The endpoint was the effects of MSCs on cognitive performance evaluated by the Morris water maze (MWM) test including escape latency, and/or number of platform crossing, and/or time in the target quadrant. Results: Nine preclinical studies incorporating 225 animals with AD were included for the meta-analysis. The studies indicated that MSC-based treatment significantly improved the learning function through measurements of the escape latency (SMD = -0.99, 95% CI = -1.33 to -0.64, p < .00001). Additionally, we observed that transplantation of MSCs significantly increased the number of platform crossing in six experiments (SMD = 0.78, 95% CI = 0.43 to 1.13, p < .0001). What's more, the times in the target quadrant were increased in five studies indicated that transplantation of MSCs could ameliorate the cognitive impairments (SMD = 1.06, 95% CI = 0.46 to 1.67, p = .0005). Conclusions: This study showed that MSC transplantation could reduce cognitive deficits in AD models. These findings support the further studies to translate MSCs in the treatment of AD in humans

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