Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP

J. Lewis, D. W. Dickson, W. L. Lin, L. Chisholm, A. Corral, G. Jones, S. H. Yen, N. Sahara, L. Skipper, D. Yager, C. Eckman, J. Hardy, M. Hutton, E. McGowan

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1185 Scopus citations


JNPL3 transgenic mice expressing a mutant tau protein, which develop neurofibrillary tangles and progressive motor disturbance, were crossed with Tg2576 transgenic mice expressing mutant β-arnyloid precursor protein (APP), thus modulating the APP-Aβ (β-arnyloid peptide) environment. The resulting double mutant (tau/APP) progeny and the Tg2576 parental strain developed Aβ deposits at the same age; however, relative to JNPL3 mice, the double mutants exhibited neurofibrillary tangle pathology that was substantially enhanced in the limbic system and olfactory cortex. These results indicate that either APP or Aβ influences the formation of neurofibrillary tangles. The interaction between Aβ and tau pathologies in these mice supports the hypothesis that a similar interaction occurs in Alzheimer's disease.

Original languageEnglish (US)
Pages (from-to)1487-1491
Number of pages5
Issue number5534
StatePublished - Aug 24 2001

ASJC Scopus subject areas

  • General


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