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Titlebook: Cell-Cycle Mechanisms and Neuronal Cell Death; Agata Copani,Ferdinando Nicoletti Book 2005 Springer-Verlag US 2005 Activation.Alzheimer.Ma

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书目名称Cell-Cycle Mechanisms and Neuronal Cell Death
编辑Agata Copani,Ferdinando Nicoletti
视频video
概述This book is comprehesive and up-to-date.Presents current views of the link between cell cycle and cell death in neurons.Includes supplementary material:
丛书名称Neuroscience Intelligence Unit
图书封面Titlebook: Cell-Cycle Mechanisms and Neuronal Cell Death;  Agata Copani,Ferdinando Nicoletti Book 2005 Springer-Verlag US 2005 Activation.Alzheimer.Ma
描述.Cell-Cycle Mechanisms and Neuronal Cell Death examines the role of cell cycle activation in the molecular mechanisms leading to neuronal degeneration. Leading Authors discuss this topic in relation to the major neurological disorders, including Alzheimer’s disease, stroke and epilepsy. This book serves to gain new insights into the molecular determinants of neuronal death and to establish new targets for therapeutic intervention. .
出版日期Book 2005
关键词Activation; Alzheimer; Mammalia; Nervous System; molecular mechanisms; neurons
版次1
doihttps://doi.org/10.1007/0-387-29390-6
isbn_softcover978-1-4899-9835-4
isbn_ebook978-0-387-29390-5Series ISSN 1431-0406
issn_series 1431-0406
copyrightSpringer-Verlag US 2005
The information of publication is updating

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Alzheimer Disease, of division, remain nonproliferative, and are terminally differentiated. Here, we review the provocative notion that, in Alzheimer disease, whole populations of nonstem cell neurons leave their quiescent state and re-enter into the cell cycle. However, such neuronal re-entry into the cell cycle is
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Offending Women in Contemporary Chinaeir relationship to other cells to reorganize their connectivity according to the requirements for information processing within a cellular network. This puts neurons on the permanent risk to erroneously convert signals derived from plastic synaptic changes into positional cues that will activate th
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Offending Women in Contemporary Chinaated as modifiers or risk factors for the disease. Although 100 years have elapsed since AD was first recognized as a separate disease entity, the last two decades have produced some of the most significant breakthroughs in our understanding of the disease. Despite this progress, the precise mechani
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https://doi.org/10.1057/9781137447180ia, and eventually die of Alzheimer’s disease. Because the gene for amyloid precursor protein (APP) resides on chromosome 21, its consequent overexpression in trisomy 21 cells presumably contributes to the development of Alzheimer’s disease in Down syndrome individuals..The connection between Down s
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