Journal
LANCET NEUROLOGY
Volume 12, Issue 6, Pages 609-622Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S1474-4422(13)70090-5
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Funding
- UK Medical Research Council [U105184291]
- Alzheimer's Research UK
- MRC [MC_U105184291, G0301152] Funding Source: UKRI
- Alzheimers Research UK [ART-PG2004A-5, ART-PG2011-20] Funding Source: researchfish
- Medical Research Council [G0301152, MC_U105184291] Funding Source: researchfish
- Parkinson"
- s UK [K-1012] Funding Source: researchfish
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The pathway leading from soluble and monomeric to hyperphosphorylated, insoluble and filamentous tau protein is at the centre of many human neurodegenerative diseases, collectively referred to as tauopathies. Dominantly inherited mutations in MAPT, the gene that encodes tau, cause forms of frontotemporal dementia and parkinsonism, proving that dysfunction of tau is sufficient to cause neurodegeneration and dementia. However, most cases of tauopathy are not inherited in a dominant manner. The first tau aggregates form in a few nerve cells in discrete brain areas. These become self propagating and spread to distant brain regions in a prion-like manner. The prevention of tau aggregation and propagation is the focus of attempts to develop mechanism-based treatments for tauopathies.
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