Jürgen Götz mainly investigates Alzheimer's disease, Genetically modified mouse, Tau protein, Neuroscience and Cell biology. His research investigates the connection between Alzheimer's disease and topics such as Hyperphosphorylation that intersect with issues in Frontotemporal lobar degeneration and Dephosphorylation. His Genetically modified mouse study introduces a deeper knowledge of Transgene.
The various areas that he examines in his Tau protein study include Molecular biology, Tauopathy and Gene isoform. His research integrates issues of Substantia nigra, Disease, Pathology and Frontotemporal dementia in his study of Neuroscience. His Cell biology study incorporates themes from Biochemistry, Neurodegeneration and Amyloid precursor protein.
Jürgen Götz mostly deals with Cell biology, Tau protein, Neuroscience, Genetically modified mouse and Disease. His study in Mutant extends to Cell biology with its themes. To a larger extent, Jürgen Götz studies Alzheimer's disease with the aim of understanding Tau protein.
His studies deal with areas such as Neurodegeneration and Frontotemporal dementia as well as Neuroscience. His Genetically modified mouse study contributes to a more complete understanding of Transgene. Jürgen Götz usually deals with Mitochondrion and limits it to topics linked to Reactive oxygen species and Oxidative phosphorylation.
Cell biology, Tauopathy, Neuroscience, Tau protein and Disease are his primary areas of study. His Cell biology research is multidisciplinary, incorporating elements of Hippocampal formation, Autophagy and Monoclonal antibody. The Tauopathy study combines topics in areas such as Frontotemporal lobar degeneration and Genetically modified mouse, Transgene.
His Neuroscience study integrates concerns from other disciplines, such as Personalized medicine, Pathogenesis and Protein folding. Tau protein is the subject of his research, which falls under Alzheimer's disease. Many of his research projects under Disease are closely connected to In patient with In patient, tying the diverse disciplines of science together.
His primary scientific interests are in Tauopathy, Cell biology, Tau protein, Alzheimer's disease and Neuroscience. His Tauopathy research incorporates elements of Therapeutic ultrasound, Genetically modified mouse, Neuropathology and Frontotemporal lobar degeneration. His work carried out in the field of Cell biology brings together such families of science as Autophagy and Transgene.
His Tau protein study combines topics in areas such as Organelle fusion, Microvesicles, Tetraspanin, Neuron and Endosome. His research in Alzheimer's disease focuses on subjects like Signal transduction, which are connected to Hyperphosphorylation. The concepts of his Neuroscience study are interwoven with issues in Protein processing, Post translational and Disease, Neurodegeneration.
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Formation of neurofibrillary tangles in P301L tau transgenic mice induced by Aβ42 fibrils
J. Götz;F. Chen;J. van Dorpe;R. M. Nitsch.
Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models
Lars M. Ittner;Yazi D. Ke;Fabien Delerue;Mian Bi.
Amyloid-β and tau — a toxic pas de deux in Alzheimer's disease
Lars M. Ittner;Jürgen Götz.
Nature Reviews Neuroscience (2011)
Animal models of Alzheimer's disease and frontotemporal dementia
Jürgen Götz;Lars M. Ittner.
Nature Reviews Neuroscience (2008)
FGF5 as a regulator of the hair growth cycle: evidence from targeted and spontaneous mutations.
Jean M. Hébert;Thomas Rosenquist;Jürgen Götz;Gail R. Martin.
Expression of amino-terminally truncated PrP in the mouse leading to ataxia and specific cerebellar lesions.
Doron Shmerling;Ivan Hegyi;Marek Fischer;Thomas Blättler.
Amyloid-β and tau synergistically impair the oxidative phosphorylation system in triple transgenic Alzheimer's disease mice
Virginie Rhein;Xiaomin Song;Andreas Wiesner;Lars M. Ittner.
Proceedings of the National Academy of Sciences of the United States of America (2009)
Somatodendritic localization and hyperphosphorylation of tau protein in transgenic mice expressing the longest human brain tau isoform.
J Götz;A Probst;M G Spillantini;T Schäfer.
The EMBO Journal (1995)
Tau Filament Formation in Transgenic Mice Expressing P301L Tau
Jürgen Götz;Feng Chen;Robi Barmettler;Roger M. Nitsch.
Journal of Biological Chemistry (2001)
Scanning ultrasound removes amyloid-β and restores memory in an Alzheimer’s disease mouse model
Gerhard Leinenga;Jürgen Götz.
Science Translational Medicine (2015)
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