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《Progress in Physiological Sciences》 2008-01
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A New Hypothesis for Early Pathogenesis in Alzheimer's Disease:Impaired Axonal Transport Mechanism

ZHU Yi-Bing1, LU Pei-Hua1, SHENG Zu-Hang1,2 (1Department of Neurobiology, JiaoTong University School of Medicine, Shanghai 200025, China; 2 Synaptic Function Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA)  
Alzheimer's disease (AD) is characterized by amyloid β (Aβ) plaques and neurofibrillary tangles in the brain, reduced synaptic density, and progressive neuronal dysfunction and loss. The elevated levels of the Aβ peptides in brain likely associated to neurodegeneration and cognitive and behavioral abnormalities. While such amyloid mechanism contributes to Alzheimer's pathological conditions, recent studies from a number of laboratories suggest that defective axonal transport may represent an early stage in AD pathogenesis because axonal swellings and reduced axonal transport were observed before apparent AD hallmarks. Here, we overview recent findings that could compromise neuronal abnormalities and provide molecular and cellular insights into the potential mechanisms underlying the defective axonal transport. We also discuss issues to be addressed in future in elucidation of the complex cellular events involved in AD pathogenesis.
【Fund】: 海外青年学者合作研究基金资助课题(39928001)
【CateGory Index】: R749.16
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