Molecular mechanisms mediating pathological plasticity in Huntington's disease and Alzheimer's disease

被引:23
作者
Spires, Tara L.
Hannan, Anthony J. [1 ]
机构
[1] Univ Melbourne, Howard Florey Inst, Parkville, Vic 3010, Australia
[2] Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Charlestown, MA USA
关键词
adult neurogenesis; Alzheimer's; Huntington's; protein aggregation; synaptic plasticity;
D O I
10.1111/j.1471-4159.2006.04275.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Neurodegenerative diseases such as Huntington's disease and Alzheimer's disease, although very different in etiology, share common degenerative processes. These include neuronal dysfunction, decreased neural connectivity, and disruption of cellular plasticity. Understanding the molecular mechanisms underlying the neural plasticity deficits in these devastating conditions may lead the way toward new therapeutic targets, both disease-specific and more generalized, which can ameliorate degenerative cognitive deficits. Furthermore, investigations of 'pathological plasticity' in these diseases lend insight into normal brain function. This review will present evidence for altered plasticity in Huntington's and Alzheimer's diseases, relate these findings to symptomatology, and review possible causes and commonalities.
引用
收藏
页码:874 / 882
页数:9
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