نتایج جستجو برای: kendalls tau

تعداد نتایج: 20931  

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2004
Bin Zhang Makoto Higuchi Yasumasa Yoshiyama Takeshi Ishihara Mark S Forman Dan Martinez Sonali Joyce John Q Trojanowski Virginia M-Y Lee

Intracellular accumulations of filamentous tau inclusions are neuropathological hallmarks of neurodegenerative diseases known as tauopathies. The discovery of multiple pathogenic tau gene mutations in many kindreds with familial frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) unequivocally confirmed the central role of tau abnormalities in the etiology of neurodegene...

2014
Katharina Flach Ellen Ramminger Isabel Hilbrich Annika Arsalan-Werner Franziska Albrecht Lydia Herrmann Michel Goedert Thomas Arendt Max Holzer

Tau is the major microtubule-associated protein in neurons involved in microtubule stabilization in the axonal compartment. Changes in tau gene expression, alternative splicing and posttranslational modification regulate tau function and in tauopathies can result in tau mislocalization and dysfunction, causing tau aggregation and cell death. To uncover proteins involved in the development of ta...

Journal: :PLoS ONE 2009
Alexis Bretteville Kunie Ando Antoine Ghestem Anne Loyens Séverine Bégard Jean-Claude Beauvillain Nicolas Sergeant Malika Hamdane Luc Buée

The role of Tau phosphorylation in neurofibrillary degeneration linked to Alzheimer's disease remains to be established. While transgenic mice based on FTDP-17 Tau mutations recapitulate hallmarks of neurofibrillary degeneration, cell models could be helpful for exploratory studies on molecular mechanisms underlying Tau pathology. Here, "human neuronal cell lines" overexpressing Wild Type or mu...

Journal: :Journal of Alzheimer's disease : JAD 2013
Félix Hernández Esther García-García Jesús Avila

Inge Grundke-Iqbal and Khalid Iqbal found a connection between microtubule associated tau and Alzheimer's disease. They described that abnormally phosphorylated tau is a component of the paired helical filaments found in the disease. Afterwards they described that tau hyperphosphorylation prevents microtubule assembly. Now trying to complement the relationship between microtubules and tau phosp...

Journal: :Human molecular genetics 2009
Yipeng Wang Marta Martinez-Vicente Ulrike Krüger Susmita Kaushik Esther Wong Eva-Maria Mandelkow Ana Maria Cuervo Eckhard Mandelkow

Aggregation and cleavage are two hallmarks of Tau pathology in Alzheimer disease (AD), and abnormal fragmentation of Tau is thought to contribute to the nucleation of Tau paired helical filaments. Clearance of the abnormally modified protein could occur by the ubiquitin-proteasome and autophagy-lysosomal pathways, the two major routes for protein degradation in cells. There is a debate on which...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2014
Marie Lise Frandemiche Sandrine De Seranno Travis Rush Eve Borel Auréliane Elie Isabelle Arnal Fabien Lanté Alain Buisson

Tau is a microtubule-associated protein well known for its stabilization of microtubules in axons. Recently, it has emerged that tau participates in synaptic function as part of the molecular pathway leading to amyloid-beta (Aβ)-driven synaptotoxicity in the context of Alzheimer's disease. Here, we report the implication of tau in the profound functional synaptic modification associated with sy...

Journal: :Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis 2014
Md Mamunul Haque Dohee Kim Young Hyun Yu Sungsu Lim Dong Jin Kim Young-Tae Chang Hyung-Ho Ha Yun Kyung Kim

Abnormal tau aggregates are presumed to be neurotoxic and are an important therapeutic target for multiple neurodegenerative disorders including Alzheimer's disease. Growing evidence has shown that tau intermolecular disulfide cross-linking is critical in generating tau oligomers that serve as a building block for higher-order aggregates. Here we report that a small molecule inhibitor prevents ...

2010
B. Aubert Y. Karyotakis J. P. Lees V. Poireau E. Prencipe X. Prudent V. Tisserand J. Garra Tico E. Grauges M. Martinelli A. Palano M. Pappagallo G. Eigen B. Stugu L. Sun M. Battaglia D. N. Brown L. T. Kerth Yu. G. Kolomensky G. Lynch I. L. Osipenkov K. Tackmann T. Tanabe N. Soni A. T. Watson H. Koch T. Schroeder D. J. Asgeirsson B. G. Fulsom C. Hearty T. S. Mattison J. A. McKenna M. Barrett A. Khan A. Randle-Conde V. E. Blinov A. D. Bukin A. R. Buzykaev V. P. Druzhinin V. B. Golubev A. P. Onuchin S. I. Serednyakov Yu. I. Skovpen E. P. Solodov M. Bondioli S. Curry I. Eschrich D. Kirkby A. J. Lankford P. Lund M. Mandelkern E. C. Martin D. P. Stoker C. A. Heusch J. Kroseberg W. S. Lockman A. J. Martinez L. Wang L. O. Winstrom C. H. Cheng T. Piatenko F. C. Porter R. Andreassen G. Mancinelli B. T. Meadows K. Mishra M. D. Sokoloff P. C. Bloom W. T. Ford A. Gaz J. F. Hirschauer M. Nagel U. Nauenberg J. G. Smith S. R. Wagner R. Ayad W. H. Toki R. J. Wilson

and |V[subscript us]| Using Tau Lepton Decays to e-[over-bar]etau, mu-[over-bar]mu, pi-tau, and K-tau Citation BABAR Collaboration et al. " Measurements of Charged Current Lepton Universality and |V_{us}| Using Tau Lepton Decays to e^{-} nu [over-bar]_{e} nu _{ tau }, mu^{-} nu [over-bar]_{mu} nu _{ tau }, pi^{-} nu _{ tau }, and K^{-} nu _{ tau }. Article is made available in accordance with t...

Journal: :American journal of neurodegenerative disease 2012
Meghan N Le Wonhee Kim Sangmook Lee Ann C McKee Garth F Hall

While the interneuronal propagation of neurofibrillary lesions in Alzheimer's disease and other tauopathies now appears to involve the spreading of tau-associated toxicity, little is known about its mechanism. We characterized the movement of human tau through the brain of a non-transgenic lower vertebrate tauopathy model in which full-length wild type and mutant human tau isoforms were express...

2016
Tong Li Kerstin E. Braunstein Juhong Zhang Ashley Lau Leslie Sibener Christopher Deeble Philip C. Wong

A central question in Alzheimer's Disease (AD) is whether the neuritic plaque is necessary and sufficient for the development of tau pathology. Hyperphosphorylation of tau is found within dystrophic neurites surrounding β-amyloid deposits in AD mouse models but the pathological conversion of tau is absent. Likewise, expression of a human tau repeat domain in mice is insufficient to drive the pa...

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