Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain

被引:2227
作者
DiFiglia, M
Sapp, E
Chase, KO
Davies, SW
Bates, GP
Vonsattel, JP
Aronin, N
机构
[1] UNIV LONDON UNIV COLL, DEPT ANAT & DEV BIOL, LONDON WC1E 6BT, ENGLAND
[2] UNITED MED & DENT SCH GUYS & ST THOMAS HOSP, GUYS HOSP, LONDON SE1 7EH, ENGLAND
[3] UNIV MASSACHUSETTS, MED CTR, DEPT MED & CELL BIOL, WORCESTER, MA 01655 USA
关键词
D O I
10.1126/science.277.5334.1990
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The cause of neurodegeneration in Huntington's disease (HD) is unknown. Patients with HD have an expanded NH2-terminal polyglutamine region in huntingtin. An NH2-terminal fragment of mutant huntingtin was localized to neuronal intranuclear inclusions (NIIs) and dystrophic neurites (DNs) in the HD cortex and striatum, which are affected in HD, and polyglutamine length influenced the extent of huntingtin accumulation in these structures. Ubiquitin was also found in NIIs and DNs, which suggests that abnormal huntingtin is targeted for proteolysis but is resistant to removal. The aggregation of mutant huntingtin may be part of the pathogenic mechanism in HD.
引用
收藏
页码:1990 / 1993
页数:4
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