亨廷顿病:免疫观点
摘要
大多数神经退行性疾病的典型特征,会导致大脑受影响区域出现一系列病理变化。HD中的神经变性也是由在聚集的
突变亨廷顿蛋白存在下的异常免疫反应引起的。免疫激活对HD神经系统的影响是一个相对未探索的研究领域。本
文总结了与HD发展和进展相关的免疫学特征。
关键词
全文:
PDF参考
[1]Huntington G. On Chorea. Medical and Surgical
Reporter of Philadelphia. 1872;26:317–321.
[2]Walker FO. Huntington’s disease. Lancet.
2007;369(9557):218–228.
[3]Purdon SE, Mohr E, Ilivitsky V, Jones BD.
Huntington’s disease: pathogenesis, diagnosis and treatment.
Journal of Psychiatry and Neuroscience. 1994;19(5):359–367.
[4]Orr AL, Li S, Wang CE, et al. N-terminal mutant
huntingtin associates with mitochondria and impairs
mitochondrial trafficking. Journal of Neuroscience.
2008;28(11):2783–2792.
[5]Reiner A, Dragatsis I, Zeitlin S, Goldowitz D. Wildtype huntingtin plays a role in brain development and neuronal
survival. Molecular Neurobiology. 2003;28(3):259–275.
[6]Ali NJ, Levine MS. 2006. Changes in expression of
N-methyl-D-aspartate receptor subunits occur early in the
R6/2 mouse model of Huntington’s disease. Dev Neurosci 28:
230–238.
[7]Andrew SE, Goldberg YP, Kremer B, Telenius H,
Theilmann J, Adam S, Starr E, Squitieri F, Lin B, Kalchman
MA. 1993. The relationship between trinucleotide (CAG)
repeat length and clinical features of Huntington’s disease.
Nat Genet 4: 398–403.
[8]MacDonald ME, Ambrose CM, Duyao MP, et al. A
novel gene containing a trinucleotide repeat that is expanded
and unstable on Huntington’s disease chromosomes. Cell.
1993;72(6):971–983.
[9]Buraczynska MJ, Van Keuren ML, Buraczynska KM,
Chang YS, Crombez E, Kurnit DM. Construction of human
embryonic cDNA libraries: HD, PKD1 and BRCA1 are
transcribed widely during embryogenesis. Cytogenetics and
Cell Genetics. 1995;71(2):197–202.
[10]Cattaneo E, Zuccato C, Tartari M. Normal huntingtin
function: an alternative approach to Huntington’s disease.
Nature Reviews Neuroscience. 2005;6(12):919–930.
DOI: http://dx.doi.org/10.12361/2705-0459-04-07-93354
Refbacks
- 当前没有refback。