Accelerated filament formation from tau protein with specific FTDP-17 missense mutations.

Article Details

Citation

Nacharaju P, Lewis J, Easson C, Yen S, Hackett J, Hutton M, Yen SH

Accelerated filament formation from tau protein with specific FTDP-17 missense mutations.

FEBS Lett. 1999 Mar 26;447(2-3):195-9.

PubMed ID
10214944 [ View in PubMed
]
Abstract

Tau is the major component of the neurofibrillar tangles that are a pathological hallmark of Alzheimers' disease. The identification of missense and splicing mutations in tau associated with the inherited frontotemporal dementia and Parkinsonism linked to chromosome 17 demonstrated that tau dysfunction can cause neurodegeneration. However, the mechanism by which tau dysfunction leads to neurodegeneration remains uncertain. Here, we present evidence that frontotemporal dementia and Parkinsonism linked to chromosome 17 missense mutations, P301L, V337M and R406W, cause an accelerated aggregation of tau into filaments. These results suggest one mechanism by which these mutations can cause neurodegeneration and frontotemporal dementia and Parkinsonism linked to chromosome 17.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Microtubule-associated protein tauP10636Details