Six tau isoforms differing in their affinity for microtubules are produced by alternative splicing from the MAPT (microtubule-associated protein tau) gene in adult human brain. Several MAPT mutations causing the familial tauopathy, FTDP-17 (frontotemporal dementia with parkinsonism linked to chromosome 17), affect alternative splicing of exon 10, encoding a microtubule-binding motif. Advanced RNA analysis methods have suggested that levels of exon 10-containing MAPT mRNA are elevated in Alzheimer's disease. Furthermore, the MAPT H1 haplotype, associated with Alzheimer's disease, promotes exon 10 inclusion in MAPT mRNA. Thus an accurate regulation of tau alternative splicing is critical for the maintenance of neuronal viability, and its alteration might be a contributing factor to Alzheimer's disease. Tau alternative splicing could represent a target for therapeutic intervention to delay the progression of pathology in familial as well as sporadic tauopathies.
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Conference Article|
July 20 2012
Tau alternative splicing in familial and sporadic tauopathies
Michael Niblock;
Michael Niblock
1Department of Clinical Neuroscience, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, U.K.
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Jean-Marc Gallo
Jean-Marc Gallo
1
1Department of Clinical Neuroscience, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, U.K.
1To whom correspondence should be addressed (emailjean-marc.gallo@kcl.ac.uk).
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Publisher: Portland Press Ltd
Received:
March 26 2012
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2012 Biochemical Society
2012
Biochem Soc Trans (2012) 40 (4): 677–680.
Article history
Received:
March 26 2012
Citation
Michael Niblock, Jean-Marc Gallo; Tau alternative splicing in familial and sporadic tauopathies. Biochem Soc Trans 1 August 2012; 40 (4): 677–680. doi: https://doi.org/10.1042/BST20120091
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