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This sirtuin gained prominence when its knockout mouse model developed severe premature aging phenotypes with mortality resulting within a month (Mostoslavsky et al., 2006).
This mouse model developed ALS-like phenotype and pathology.
Finally, of considerable interest and wide attention is the triple tg mouse model developed by LaFerla et al.
However, no mouse model developed thus far recapitulates all of these characteristics or exactly mimics what is seen in human cGvHD.
Three reports have employed electrophysiological methods to examine intrinsic and synaptic properties in the mouse model developed by Koike et al. (2006).
For example, 26S proteasome dysfunction was sufficient to trigger neurodegenerative disease in a transgenic mouse model developed by conditionally depleting a 26S proteasome subunit in forebrain neurons.
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The 3xTg-AD mouse model develops both Aβ plaques and neurofibrillary tangles, the neuro-pathological hallmarks of AD, by 6 months of age, but no research has investigated the age-related changes in WM in these mice.
3xTg-AD mouse model develops two age-related neuropathological features associated with AD, amyloid plaques and neurofibrillary tangle formation, as well as age-related behavioral deficits that correlate with the neuropathology.
The FFD mouse model develops features of human NAFLD.
The Peg3 knock-out mouse model develops increased adiposity despite lower food intake.
This mouse model develops lung adenocarcinomas with a high incidence of metastases and gender differences in cancer-related death.
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