Evidence for abnormal tau phosphorylation in early aggressive multiple sclerosis |
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Authors: | Jane Marian Anderson Rickie Patani Richard Reynolds Richard Nicholas Alastair Compston Maria Grazia Spillantini Siddharthan Chandran |
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Institution: | (1) Cambridge Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Forvie Site, Robinson Way, Cambridge, UK;(2) Department of Cellular and Molecular Neuroscience, Imperial College Faculty of Medicine, Charing Cross Hospital Campus, Fulham Palace Road, London, UK |
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Abstract: | 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.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
J. M. Anderson and R. Patani are co-first authors. |
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Keywords: | Tau Acute inflammatory demyelinating disease Experimental autoimmune encephalomyelitis Axonopathy Neuronal loss |
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