Can the calcium hypothesis explain synaptic loss in Alzheimer's disease?
Can the calcium hypothesis explain synaptic loss in Alzheimer's disease?
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DOI:
10.1159/000354778
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发表时间:
2014
期刊:
影响因子:
--
通讯作者:
Bezprozvanny I
中科院分区:
文献类型:
--
作者:
Popugaeva E;Bezprozvanny I
Alzheimer’s disease (AD) is the threat of modern humankind that is provoked by increased human lifespan. Despite extensive studies on AD pathology for more than 100 years there are no disease preventing therapies. Growing evidence suggests the role of calcium (Ca2+) in the pathogenesis of AD. The main purpose of the article is to understand whether modern science is able to explain the synapse loss observed in early AD and discuss the role of Ca2+ hypothesis in it. Based on results obtained in our laboratory and others we propose that familial AD-associated mutations in presenilins cause Ca2+ overload of endoplasmic reticulum stores which leads to compensatory downregulation of neuronal store-operated Ca2+ (nSOC) entry pathway. We propose that synaptic nSOC is necessary for stability of mature synaptic spines and that dysfunction of this pathway may play an important role in synaptic and memory loss in AD.
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The Journal of neuroscience : the official journal of the Society for Neuroscience
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10.1523/jneurosci.1554-10.2010
发表时间:
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The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
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通讯作者:
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