期刊
ACTA NEUROPATHOLOGICA
卷 117, 期 5, 页码 583-589出版社
SPRINGER
DOI: 10.1007/s00401-009-0515-2
关键词
Tau; Acute inflammatory demyelinating disease; Experimental autoimmune encephalomyelitis; Axonopathy; Neuronal loss
资金
- Webb Trust Fund
- Husky Foundation
- Sir David Walker Trust Fund
- Medical Research Council
- Wellcome Trust and MS Society of Great Britain and Northern Ireland
- National Multiple Sclerosis Society, USA
- Multiple Sclerosis Society of Great Britain and Northern Ireland [207495]
- Medical Research Council [G0700356] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0508-10335] Funding Source: researchfish
Although progression in multiple sclerosis is pathologically dominated by neurodegeneration, the underlying mechanism is unknown. Abnormal hyperphosphorylation of tau is implicated in the aetiopathogenesis of some common neurodegenerative disorders. We recently demonstrated the association of insoluble tau with established secondary progressive MS, raising the hypothesis that its accumulation is relevant to disease progression. In order to begin to determine the temporal emergence of abnormal tau with disease progression in MS, we examined tau phosphorylation in cerebral tissue from a rare case of early aggressive MS. We report tau hyperphosphorylation occurring in multiple cell types, with biochemical analysis confirming restriction to the soluble fraction. The absence of sarcosyl-insoluble tau fraction in early disease and its presence in secondary progression raises the possibility that insoluble tau accumulates with disease progression.
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