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Related Experiment Videos

FTDP-17 tau mutations decrease the susceptibility of tau to calpain I digestion.

S Yen1, C Easson, P Nacharaju

  • 1Department of Pharmacology, Birdsall Medical Research Building, Mayo Clinic Jacksonville, FL 32224, USA.

FEBS Letters
|November 24, 1999
PubMed
Summary
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Mutations in the tau gene cause Frontotemporal Dementia and Parkinsonism linked to chromosome 17 (FTDP-17). Certain tau mutations reduce degradation, leading to tau accumulation and disease pathogenesis.

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17) is a neurodegenerative disease.
  • It is characterized by the accumulation of filamentous tau in the brain.
  • FTDP-17 is caused by mutations in the tau gene.

Purpose of the Study:

  • To investigate the proteolytic degradation of specific tau mutations associated with FTDP-17.
  • To determine if reduced degradation contributes to tau accumulation in FTDP-17.

Main Methods:

  • Assessed the susceptibility of wild-type and mutant tau proteins (V337M, R406W, P301L) to degradation by calpain I.
  • Analyzed the accessibility of a specific cleavage site on the tau protein.

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Main Results:

  • Mutants V337M and R406W showed reduced susceptibility to calpain I degradation compared to mutant P301L and wild-type tau.
  • This difference was partly due to altered accessibility of a cleavage site near the carboxy-terminus.

Conclusions:

  • Decreased proteolytic degradation of tau may play a role in the pathogenesis of some forms of FTDP-17.
  • Specific tau mutations can impair degradation pathways, leading to protein accumulation.