H-Index & Metrics Best Publications

H-Index & Metrics

Discipline name H-index Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 52 Citations 9,406 138 World Ranking 8863 National Ranking 248

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • Internal medicine

His primary areas of investigation include Neuroscience, Alzheimer's disease, Cell biology, Disease and Tau protein. His Neuroscience study incorporates themes from Substantia nigra, Transgene and Frontotemporal dementia. His Frontotemporal dementia research includes elements of Axoplasmic transport, Genetically modified mouse and Trinucleotide repeat expansion.

Lars M. Ittner has researched Alzheimer's disease in several fields, including Endocrinology, Crosstalk and Degenerative disease. His work carried out in the field of Cell biology brings together such families of science as Excitotoxicity and Postsynaptic potential. His Disease research is multidisciplinary, incorporating perspectives in Neuroprotection and Molecular pathway.

His most cited work include:

  • Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models (1251 citations)
  • Amyloid-β and tau — a toxic pas de deux in Alzheimer's disease (884 citations)
  • Animal models of Alzheimer's disease and frontotemporal dementia (539 citations)

What are the main themes of his work throughout his whole career to date?

Lars M. Ittner mainly investigates Genetically modified mouse, Neuroscience, Cell biology, Transgene and Disease. His Genetically modified mouse research integrates issues from Endocrinology, Tau protein, Pathology, Internal medicine and Tauopathy. His Neuroscience research incorporates elements of Dementia, Frontotemporal dementia, Amyotrophic lateral sclerosis, Excitotoxicity and Alzheimer's disease.

His study in Cell biology is interdisciplinary in nature, drawing from both Gene expression and Immunology. His biological study deals with issues like Molecular biology, which deal with fields such as Calcitonin gene-related peptide. His research in Disease intersects with topics in Treatment strategy and Pathological.

He most often published in these fields:

  • Genetically modified mouse (43.16%)
  • Neuroscience (41.03%)
  • Cell biology (36.75%)

What were the highlights of his more recent work (between 2016-2021)?

  • Neuroscience (41.03%)
  • Genetically modified mouse (43.16%)
  • Tau protein (22.65%)

In recent papers he was focusing on the following fields of study:

His main research concerns Neuroscience, Genetically modified mouse, Tau protein, Disease and Cell biology. His Neuroscience research includes themes of Alzheimer's disease, Phenotype, Hyperphosphorylation and Excitotoxicity. Genetically modified mouse is the subject of his research, which falls under Transgene.

His Transgene research incorporates themes from Amyotrophic lateral sclerosis, Neurodegeneration and Pathology. The various areas that Lars M. Ittner examines in his Disease study include Epothilone D and Pharmacology. The Cell biology study combines topics in areas such as Tissue engineering, Cell culture and Gene expression.

Between 2016 and 2021, his most popular works were:

  • The Link between Type 2 Diabetes and Neurodegeneration: Roles for Amyloid-β, Amylin, and Tau Proteins (84 citations)
  • Dendritic Tau in Alzheimer's Disease. (83 citations)
  • Dendritic Tau in Alzheimer's Disease. (83 citations)

In his most recent research, the most cited papers focused on:

  • Gene
  • Enzyme
  • Internal medicine

Lars M. Ittner mainly focuses on Neuroscience, Disease, Tau protein, Alzheimer's disease and Frontotemporal dementia. His studies in Neuroscience integrate themes in fields like Neuroinflammation, Amyotrophic lateral sclerosis, Neurodegeneration and MAPK/ERK pathway. Disease is a subfield of Pathology that Lars M. Ittner studies.

His research integrates issues of Genetically modified mouse and Viral vector in his study of Pathology. In his study, Amyloid is inextricably linked to Endocrinology, which falls within the broad field of Alzheimer's disease. The study incorporates disciplines such as Neuropathology and Pathological in addition to Frontotemporal dementia.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models

Lars M. Ittner;Yazi D. Ke;Fabien Delerue;Mian Bi.
Cell (2010)

1585 Citations

Amyloid-β and tau — a toxic pas de deux in Alzheimer's disease

Lars M. Ittner;Jürgen Götz.
Nature Reviews Neuroscience (2011)

1234 Citations

Animal models of Alzheimer's disease and frontotemporal dementia

Jürgen Götz;Lars M. Ittner.
Nature Reviews Neuroscience (2008)

759 Citations

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)

592 Citations

Toll-like receptor engagement converts T-cell autoreactivity into overt autoimmune disease.

Karl S Lang;Mike Recher;Tobias Junt;Alexander A Navarini.
Nature Medicine (2005)

416 Citations

Sodium selenate mitigates tau pathology, neurodegeneration, and functional deficits in Alzheimer's disease models

Janet van Eersel;Yazi D. Ke;Xin Liu;Fabien Delerue.
Proceedings of the National Academy of Sciences of the United States of America (2010)

265 Citations

Tau aggregation and its interplay with amyloid-β.

Rebecca M. Nisbet;Juan‑Carlos Polanco;Lars M. Ittner;Jürgen Götz.
Acta Neuropathologica (2015)

249 Citations

Neural crest stem cell maintenance by combinatorial Wnt and BMP signaling.

Maurice Kléber;Hye-Youn Lee;Heiko Wurdak;Johanna Buchstaller.
Journal of Cell Biology (2005)

220 Citations

Neuronal MicroRNA Deregulation in Response to Alzheimer's Disease Amyloid-β

Nicole Schonrock;Yazi D. Ke;David Humphreys;Matthias Staufenbiel.
PLOS ONE (2010)

211 Citations

Parkinsonism and impaired axonal transport in a mouse model of frontotemporal dementia.

Lars M. Ittner;Thomas Fath;Yazi D. Ke;Mian Bi.
Proceedings of the National Academy of Sciences of the United States of America (2008)

206 Citations

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