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NTIS 바로가기Aging cell, v.18 no.1, 2019년, pp.e12860 -
Wang, Zhao‐Tao (Department of Neurosurgery Affiliated Bayi Brain Hospital, General Army Hospital Southern Medical University Beijing China) , Lu, Mei‐Hong (Jiangsu Key Laboratory of Neuropsychiatric Diseases, Institute of Neuroscience Soochow University Suzhou China) , Zhang, Yan (Department of Neurosurgery Affiliated Bayi Brain Hospital, General Army Hospital Southern Medical University Beijing China) , Ji, Wen‐Li (Jiangsu Key Laboratory of Neuropsychiatric Diseases, Institute of Neuroscience Soochow University Suzhou China) , Lei, Lei (Department of Physiology, Liaoning Provincial Key Laboratory of Cerebral Diseases Dalian Medical University Dalian China) , Wang, Wang (Jiangsu Key Laboratory of Neuropsychiatric Diseases, Institute of Neuroscience Soochow University Suzhou China) , Fang, Li‐Pao (Jiangsu Key Laboratory of Neuropsychiatric Diseases, Institute of Neuroscience Soochow University Suzhou China China<) , Wang, Lu‐Wen , Yu, Fan , Wang, Ji , Li, Zhen‐Yu , Wang, Jian‐Rong , Wang, Ting‐Hua , Dou, Fei , Wang, Qin‐Wen , Wang, Xing‐Long , Li, Shao , Ma, Quan‐Hong , Xu, Ru‐Xiang
AbstractMitochondrial dysfunction is an early feature of Alzheimer's disease (AD). Accumulated damaged mitochondria, which are associated with impaired mitophagy, contribute to neurodegeneration in AD. We show levels of Disrupted‐in‐schizophrenia‐1 (DISC1), which is genetically ...
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