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Alzheimer's disease: synapses gone cold

来自 EBSCO

阅读量：

86

作者：

RM Koffie，BT Hyman，TL Spires-Jones

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摘要：

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by insidious cognitive decline and memory dysfunction. Synapse loss is the best pathological correlate of cognitive decline in AD and mounting evidence suggests that AD is primarily a disease of synaptic dysfunction. Soluble oligomeric forms of amyloid beta (A??), the peptide that aggregates to form senile plaques in the brain of AD patients, have been shown to be toxic to neuronal synapses both in vitro and in vivo. A?? oligomers inhibit long-term potentiation (LTP) and facilitate long-term depression (LTD), electrophysiological correlates of memory formation. Furthermore, oligomeric A?? has also been shown to induce synapse loss and cognitive impairment in animals. The molecular underpinnings of these observations are now being elucidated, and may provide clear therapeutic targets for effectively treating the disease. Here, we review recent findings concerning AD pathogenesis with a particular focus on how A?? impacts synapses.

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关键词：

long-term depression long-term potentiation synapse loss Alzheimer's disease amyloid-beta cognitive decline Neuroscience Neurosurgery

DOI：

10.1186/1750-1326-6-63

被引量：

621

年份：

2011

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来源期刊

Molecular Neurodegeneration,6,1(2011-08-26)
2011-08-26

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2013
被引量：136

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