Convergent pathogenic pathways in Alzheimer's and Huntington's diseases: shared targets for drug development

被引:64
作者
Ehrnhoefer, Dagmar E. [1 ]
Wong, Bibiana K. Y. [1 ]
Hayden, Michael R. [1 ]
机构
[1] Univ British Columbia, Ctr Mol Med & Therapeut, Dept Med Genet, Child & Family Res Inst, Vancouver, BC V5Z 4H4, Canada
基金
奥地利科学基金会;
关键词
UBIQUITIN-PROTEASOME SYSTEM; AMYLOID PRECURSOR PROTEIN; MILD COGNITIVE IMPAIRMENT; LONG-TERM POTENTIATION; NERVE GROWTH-FACTOR; NEUROTROPHIC FACTOR; MOUSE MODEL; MUTANT HUNTINGTIN; TRANSGENIC MICE; EPIGALLOCATECHIN-3-GALLATE EGCG;
D O I
10.1038/nrd3556
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Neurodegenerative diseases, exemplified by Alzheimer's disease and Huntington's disease, are characterized by progressive neuropsychiatric dysfunction and loss of specific neuronal subtypes. Although there are differences in the exact sites of pathology, and the clinical profiles of these two conditions only partially overlap, considerable similarities in disease mechanisms and pathogenic pathways can be observed. These shared mechanisms raise the possibility of exploiting common therapeutic targets for drug development. As Huntington's disease has a monogenic cause, it is possible to accurately identify individuals who carry the Huntington's disease mutation but do not yet manifest symptoms. These individuals could act as a model for Alzheimer's disease to test therapeutic interventions that target shared pathogenic pathways.
引用
收藏
页码:853 / 867
页数:15
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