期刊
BRAIN
卷 131, 期 -, 页码 1736-1748出版社
OXFORD UNIV PRESS
DOI: 10.1093/brain/awn119
关键词
tau; secondary progressive multiple sclerosis; experimental autoimmune encephalomyelitis; axonopathy; neuronal loss
资金
- Medical Research Council [MC_U105184319, G9828345] Funding Source: researchfish
- MRC [G9828345, MC_U105184319] Funding Source: UKRI
- Medical Research Council [G9828345, MC_U105184319] Funding Source: Medline
- Multiple Sclerosis Society [835] Funding Source: Medline
The pathological correlate of clinical disability and progression in multiple sclerosis is neuronal and axonal loss; however, the underlying mechanisms are unknown. Abnormal phosphorylation of tau is a common feature of some neurodegenerative disorders, such as Alzheimers disease. We investigated the presence of tau hyperphosphorylation and its relationship with neuronal and axonal loss in chronic experimental autoimmune encephalomyelitis (CEAE) and in brain samples from patients with secondary progressive multiple sclerosis. We report the novel finding of abnormal tau phosphorylation in CEAE. We further show that accumulation of insoluble tau is associated with both neuronal and axonal loss that correlates with progression from relapsingremitting to chronic stages of EAE. Significantly, analysis of secondary progressive multiple sclerosis brain tissue also revealed abnormally phosphorylated tau and the formation of insoluble tau. Together, these observations provide the first evidence implicating abnormal tau in the neurodegenerative phase of tissue injury in experimental and human demyelinating disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据