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Recent progress in the study of intracellular toxicity of amyloid p peptide in Alzheimer's disease

progress in Natural Science:Materials International 2007年第3期 233-236页

作者： ZHANG Yan and YU Longchuan (College of Life Sciences, peking University, Beijing 100871, China)

amyloidβ(Aβ) deposition is one of the major pathological markers of Alzheimer’s disease (AD). Extracellular Afi toxi-city has been studied for a long time in AD research field. However, controversial data show that extracellular Aβload does not correlate with the dementia levels of AD patients and extracellular Aβonly induces significant cell death at non-physiological high concentrations. With the evolvement of Afi hypothesis, considerable attention has been devoted to the study of intracellular Aβtoxicity recently. Intracellular Aβinduces dramatic cell loss in AD transgenic models and in human primary neurons (at pM concentrations) through p53, Bax and caspase-6 pathways. Here, we review the generation, toxicity and possible pathways of intracellular Aβtoxicity, and discuss the implication and current knowledge of intracellular Aβin neuronal cell loss in neurodegenerative diseases.

关键词： Alzheimer’s disease amyloid p peptide neruonal loss.

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Transplantation of bone marrow mesenchymal stem cells improves cognitive deficits and alleviates neuropathology in animal models of Alzheimer’s disease: a meta-analytic review on potential mechanisms

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Translational Neurodegeneration 2020年第2期9卷 214-233页

作者： Chuan Qin Yalan Lu Kewei Wang Lin Bai Guiying Shi Yiying Huang Yongning Li Institute of Laboratory Animal Sciences Chinese Academy of Medical Sciences&Comparative Medical CenterPeking Union Medical CollegeBeijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases5 Panjiayuan Nanli StBeijing100021China Department of International Medical Service&Department of Neurosurgery Peking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeShuaifuyuan 1Dong Cheng DistrictBeijing100730China

Background Alzheimer’s disease is a neurodegenerative disorder.Therapeutically,a transplantation of bone marrow mesenchymal stem cells(BMMSCs)can play a beneficial role in animal models of Alzheimer’s disease.However,the relevant mechanism remains to be fully elucidated.Main body Subsequent to the transplantation of BMMSCs,memory loss and cognitive impairment were significantly improved in animal models with Alzheimer’s disease(AD).potential mechanisms involved neurogenesis,apoptosis,angiogenesis,inflammation,immunomodulation,etc.The above mechanisms might play different roles at certain stages.It was revealed that the transplantation of BMMSCs could alter some gene levels.Moreover,the differential expression of representative genes was responsible for neuropathological phenotypes in Alzheimer’s disease,which could be used to construct gene-specific patterns.Conclusions Multiple signal pathways involve therapeutic mechanisms by which the transplantation of BMMSCs improves cognitive and behavioral deficits in AD models.Gene expression profile can be utilized to establish statistical regression model for the evaluation of therapeutic effect.The transplantation of autologous BMMSCs maybe a prospective therapy for patients with Alzheimer’s disease.

关键词： Alzheimer's disease Bone marrow mesenchymal stem cells Meta-analysis amyloid p peptide Memory loss Cognitive deficits Animal model Neuropathology

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