Tauopathy in Drosophila: Neurodegeneration Without Neurofibrillary Tangles

By Curtis W. Wittmann, M. Wszolek, J. Shulman, P. Salvaterra, Jada Lewis, M. Hutton, M. Feany. Science, 2001

957 citations recorded by the source corpus.

Subfields: Cell Biology, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/a2c5462e925555e821710728b9981fc976a07ac3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

In Pharmacology

In Physiology

Citations in the corpus

Mechanisms of tau-induced neurodegeneration (2009, neutral): “In wild-type human tau- and mutated human tau-transgenic drosophila, the accumulation of the abnormally phosphorylated tau in the absence of its fibrillization into neurofibrillary tangles leads to neurodegeneration [208].”
Death by necrosis (2002, background): “Expression of either the wild-type or mutant forms of these two proteins in Drosophila faithfully reproduces features of the human neurodegenerative conditions associated with them (Feany and Bender, 2000; Wittmann et al., 2001; see Supplementary data available at EMBO reports Online).”
Animal models of Alzheimer's disease and frontotemporal dementia (2008, background): “Expression of either WT or R406W human tau in flies produces adult onset, progressive neurodegeneration and premature death, and enhances the accumulation and toxicity of FTDP-17 tau expressed panneuronally or in cholinergic neuron”
Neurodegenerative diseases: a decade of discoveries paves the way for therapeutic breakthroughs (2004, background): “Interestingly, in Drosophila, neurodegeneration was linked to the overexpression of tau, but in the absence of neurofibrillary patholog”
The Fly as a Model for Neurodegenerative Diseases: Is It Worth the Jump? (2007, positive): “showed that expression of human APP in the eye alone, or in combination with human β-secretase, resulted in progressive degeneration of retinal photoreceptors and age-dependent Aβ plaque formation. Both phenotypes were completely absent when β-secretase was expressed alone. Moreover, when APP, β-sec”
Aberrant Cdk5 activation by p25 triggers pathological events leading to neurodegeneration and neurofibrillary tangles. (2003, background): “These findings also provide evidence for the involvement of p25/Cdk5 in activating other kinases that ported by a fly model of tauopathy (Wittmann et al., 2001) and some human patients with frontotemporal lead to tau hyperphosphorylation.”
Rapamycin alleviates toxicity of different aggregate-prone proteins. (2006, result): “In this Drosophila model, independent insertions of EGFPNLS-A37 cause toxicity in a variety of tissues when expressed Downloaded from https://academic.oup.com/hmg/article-abstract/15/3/433/630542 by guest on 27 July 2018 at similar levels to EGFP-NLS-A7 insertions, which are not toxic (Berger Z. et ”
Tau blocks traffic of organelles, neurofilaments, and APP vesicles in neurons and enhances oxidative stress (2002, background): “, 2001), and tau-overexpressing flies also show defects in neuronal traffic without evidence of tau aggregation (Wittmann et al., 2001).”
Tau in Alzheimer Disease and Related Tauopathies (2010, background): “In wild-type human tau- and mutated human tau-transgenic drosophila, the accumulation of the abnormally phosphorylated tau in the absence of its fibrillization into neurofibrillary tangles leads to neurodegeneration [56].”
Role of tau protein in both physiological and pathological conditions. (2004, background): “Transgenic flies expressing human wild-type and mutant tau (R406W) both die prematurely (299), although the toxicity of the mutant tau was higher than the wildtype.”
Abundant Tau Filaments and Nonapoptotic Neurodegeneration in Transgenic Mice Expressing Human P301S Tau Protein (2002, background): “In contrast, in Drosophila melanogaster expressing either wild-type or mutant human tau, nerve cell death by apoptosis was found in the apparent absence of tau filaments (Wittmann et al., 2001; Jackson et al., 2002).”