Formation of Neurofibrillary Tangles in P301L Tau Transgenic Mice Induced by Aβ42 Fibrils

  • J. Götz
    Division of Psychiatry Research, University of Zürich, August Forel Strasse 1, 8008 Zürich, Switzerland.
  • F. Chen
    Division of Psychiatry Research, University of Zürich, August Forel Strasse 1, 8008 Zürich, Switzerland.
  • J. van Dorpe
    Experimental Genetics Group, Center for Human Genetics, K. U. Leuven, Campus Gasthuisberg, Leuven, Belgium.
  • R. M. Nitsch
    Division of Psychiatry Research, University of Zürich, August Forel Strasse 1, 8008 Zürich, Switzerland.

抄録

<jats:p> β-Amyloid plaques and neurofibrillary tangles (NFTs) are the defining neuropathological hallmarks of Alzheimer's disease, but their pathophysiological relation is unclear. Injection of β-amyloid Aβ <jats:sub>42</jats:sub> fibrils into the brains of P301L mutant tau transgenic mice caused fivefold increases in the numbers of NFTs in cell bodies within the amygdala from where neurons project to the injection sites. Gallyas silver impregnation identified NFTs that contained tau phosphorylated at serine 212/threonine 214 and serine 422. NFTs were composed of twisted filaments and occurred in 6-month-old mice as early as 18 days after Aβ <jats:sub>42</jats:sub> injections. Our data support the hypothesis that Aβ <jats:sub>42</jats:sub> fibrils can accelerate NFT formation in vivo. </jats:p>

収録刊行物

  • Science

    Science 293 (5534), 1491-1495, 2001-08-24

    American Association for the Advancement of Science (AAAS)

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