Premium
P1–050: Beta–amyloid accumulation in cerebral cortex is altered in transgenic Tg2576 mice deficient of c–Jun N–terminal kinase
Author(s) -
Schliebs Reinhard,
Schulze Ute,
Heinitz Katrin,
Kouznetsova Elena,
Castro Lourdes,
Herdegen Thomas,
Peinado Maria Angeles
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.425
Subject(s) - genetically modified mouse , oxidative stress , amyloid precursor protein , kinase , transgene , cerebral cortex , chemistry , amyloid beta , gene isoform , presenilin , alzheimer's disease , biology , endocrinology , medicine , microbiology and biotechnology , biochemistry , gene , disease , peptide
tion, a progressive neurogenic muscle atrophy with an axonal loss in peripheral nerves was documented. Conclusions: Thus, depending on the cell type, tau aggregation leads to at least two kinds of pathology. Indeed, these transgenic mice develop an Alzheimer-like neurofibrillary pathology predominantly in the telencephalon, and an axonopathy with neurofilament-rich inclusions affecting predominantly the spinal motor neurons. This transgenic model will be useful for the study of tauopathies characterized by both frontotemporal degeneration and motor neuron disease.