Abundant Tau Filaments and Nonapoptotic Neurodegeneration in Transgenic Mice Expressing Human P301S Tau Protein
By B. Allen, E. Ingram, M. Takao, Michael J. Smith, R. Jakes, K. Virdee, H. Yoshida, M. Holzer, M. Craxton, P. Emson and 6 more. Journal of Neuroscience, 2002
705 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/387bed19e93ace7ab03da8ffbe827e72bd257781
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Citations in the corpus
- Brain homogenates from human tauopathies induce tau inclusions in mouse brain (2013, methodology): “Line ALZ17 expressing human wild-type four-repeat tau (19), mice transgenic for human mutant P301S tau (15), line APP23 expressing human mutant amyloid precursor protein (48), and nontransgenic control mice, all females on the C57BL/6 background, were used.”
- Role of tau protein in both physiological and pathological conditions. (2004, background): “More recently, another transgenic mouse containing the P301L mutation has been characterized (249), as well as one containing the P301S mutation (4).”
- Age-Dependent Neurofibrillary Tangle Formation, Neuron Loss, and Memory Impairment in a Mouse Model of Human Tauopathy (P301L) (2005, background): “This phenomenon has been described in models expressing P301L, P301S, and non-mutant human tau (Lewis et al., 2000; Allen et al., 2002; Terwel et al., 2005).”
- GSK3 inhibitors: development and therapeutic potential (2004, result): “This contrasts with other transgenic lines that replicate the essential molecular and cellular features of human tauopathies, including the formation of abundant filaments made of hyperphosphorylated tau protein and non-apoptotic loss of nerve cell”
- Aberrant Cdk5 activation by p25 triggers pathological events leading to neurodegeneration and neurofibrillary tangles. (2003, background): “…Cdk5 activity, does not lead to tau hyperphosphorylation (Van den Haute et al., 2001). ing human mutations of tau found in frontotemporal dementias (Allen et al., 2002; Lewis et al., 2000; NobleWe also find that p25 Tg mice do not display increases in phosphorylation of Nudel, mDab1, and PSD95,…”
- Neuronal Cell Death. (2018, neutral): “While neuronal death is prevalent in transgenic tauopathy mouse models, none is evidently purely apoptotic (10, 186).”