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Truncated tau from sporadic Alzheimer's disease suffices to drive neurofibrillary degeneration in vivo.

Truncated tau protein is the characteristic feature of human sporadic Alzheimer's disease. We have identified truncated tau proteins conformationally different from normal healthy tau. Subpopulations of these structurally different tau species promoted abnormal microtubule assembly in vitro suggesting toxic gain of function. To validate pathological activity in vivo we expressed active form of human truncated tau protein as transgene, in the rat brain. Its neuronal expression led to the development of the neurofibrillary degeneration of Alzheimer's type. Furthermore, biochemical analysis of neurofibrillary changes revealed that massive sarcosyl insoluble tau complexes consisted of human Alzheimer's tau and endogenous rat tau in ratio 1:1 including characteristic Alzheimer's disease (AD)-specific proteins (A68). This work represents first insight into the possible causative role of truncated tau in AD neurofibrillary degeneration in vivo.

Pubmed ID: 16753151

Authors

  • Zilka N
  • Filipcik P
  • Koson P
  • Fialova L
  • Skrabana R
  • Zilkova M
  • Rolkova G
  • Kontsekova E
  • Novak M

Journal

FEBS letters

Publication Data

June 26, 2006

Associated Grants

None

Mesh Terms

  • Alzheimer Disease
  • Animals
  • Animals, Genetically Modified
  • Brain
  • Humans
  • Microtubules
  • Nerve Degeneration
  • Protein Binding
  • Rats
  • Solubility
  • Spinal Cord
  • tau Proteins