From understanding synaptic plasticity to the development of cognitive enhancers

被引:17
|
作者
Cheung, Zelda H.
Ip, Nancy Y. [1 ]
机构
[1] Hong Kong Univ Sci & Technol, Div Life Sci, State Key Lab Mol Neurosci, Kowloon, Hong Kong, Peoples R China
来源
关键词
Alzheimer's disease; BDNF; dendritic spines; depression; synaptic plasticity; DENDRITIC SPINE LOSS; NMDA RECEPTOR TRAFFICKING; ALZHEIMERS-DISEASE; STRUCTURAL PLASTICITY; NEUROTROPHIC FACTOR; AMYLOID-BETA; MOLECULAR-MECHANISMS; PROTEIN-SYNTHESIS; MESSENGER-RNAS; STRESS;
D O I
10.1017/S1461145710001537
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Accumulating evidence reveals that synaptic dysfunction precedes neuronal loss in neurodegenerative diseases such as Alzheimer's disease. Intriguingly, synaptic abnormality is also implicated in a myriad of psychiatric disorders including depression. In particular, alterations in spine density and morphology have been associated with aberrant synaptic activity in these diseased brains. Understanding the molecular mechanisms underlying the regulation of spine morphogenesis, synaptic function and plasticity under physiological and pathological conditions will therefore provide critical insights for the development of potential therapeutic agents against these diseases. Here we summarize existing knowledge on some of the molecular players in synaptic plasticity, and highlight how these findings from basic neuro-scientific research aid in the identification of novel drug leads for the development of therapeutics.
引用
收藏
页码:1247 / 1256
页数:10
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