D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Medicine D-index 74 Citations 23,591 180 World Ranking 14967 National Ranking 7679

Research.com Recognitions

Awards & Achievements

Member of the Association of American Physicians

Overview

What is he best known for?

The fields of study J. Timothy Greenamyre is best known for:

  • Gene
  • Dopamine
  • Enzyme

Glutamate receptor and NMDA receptor are the main topics of his Receptor study. His studies link Receptor with Glutamate receptor. His study in Alzheimer's disease extends to Disease with its themes. His research on Neuroscience frequently links to adjacent areas such as Neuroprotection. J. Timothy Greenamyre performs integrative study on Mitochondrion and Gene. J. Timothy Greenamyre incorporates Gene and Disease in his research. His Toxicity research extends to Internal medicine, which is thematically connected. His Toxicity study frequently draws parallels with other fields, such as Internal medicine. His multidisciplinary approach integrates Parkinson's disease and Alpha-synuclein in his work.

His most cited work include:

  • Chronic systemic pesticide exposure reproduces features of Parkinson's disease (3186 citations)
  • Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines (922 citations)
  • Mechanism of Toxicity in Rotenone Models of Parkinson's Disease (851 citations)

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

His work blends Neuroscience and Pharmacology studies together. He merges Pharmacology with Neuroscience in his research. Disease is closely attributed to Neurodegeneration in his study. His Neurodegeneration study frequently draws connections to other fields, such as Pathology. Many of his studies on Pathology apply to Parkinson's disease as well. By researching both Parkinson's disease and Dopaminergic, he produces research that crosses academic boundaries. J. Timothy Greenamyre combines Dopaminergic and Substantia nigra in his research. His Substantia nigra study often links to related topics such as Disease. J. Timothy Greenamyre merges Biochemistry with Enzyme in his research.

J. Timothy Greenamyre most often published in these fields:

  • Neuroscience (63.28%)
  • Disease (62.71%)
  • Biochemistry (51.98%)

What were the highlights of his more recent work (between 2017-2022)?

  • Disease (86.96%)
  • Neuroscience (78.26%)
  • Parkinson's disease (73.91%)

In recent works J. Timothy Greenamyre was focusing on the following fields of study:

The research on Mitochondrial DNA and Messenger RNA is part of his Gene project. J. Timothy Greenamyre regularly links together related areas like Genetics in his Messenger RNA studies. He merges many fields, such as Genetics and Mitochondrial DNA, in his writings. His Disease study frequently draws connections between related disciplines such as LRRK2. As part of his studies on LRRK2, he frequently links adjacent subjects like Pathology. J. Timothy Greenamyre performs integrative Pathology and Pathogenesis research in his work. J. Timothy Greenamyre performs multidisciplinary studies into Pathogenesis and Disease in his work. J. Timothy Greenamyre conducts interdisciplinary study in the fields of Neuroscience and Cell biology through his works. His Cell biology study frequently draws connections between related disciplines such as Rotenone.

Between 2017 and 2022, his most popular works were:

  • LRRK2 activation in idiopathic Parkinson’s disease (311 citations)
  • Revisiting protein aggregation as pathogenic in sporadic Parkinson and Alzheimer diseases (171 citations)
  • Astrocyte-specific DJ-1 overexpression protects against rotenone-induced neurotoxicity in a rat model of Parkinson's disease (63 citations)

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

  • Gene
  • Parkinson's disease
  • Neurodegeneration

Neuroscience is closely attributed to Astrocyte in his work. His studies link Neuroscience with Astrocyte. As part of his studies on Pathology, J. Timothy Greenamyre frequently links adjacent subjects like Amyloid (mycology). His research on Amyloid (mycology) often connects related areas such as Pathology. In his research, J. Timothy Greenamyre undertakes multidisciplinary study on Disease and Etiology. J. Timothy Greenamyre carries out multidisciplinary research, doing studies in Etiology and Pathogenesis. Much of his study explores Pathogenesis relationship to Immunology. J. Timothy Greenamyre integrates many fields in his works, including Immunology and Genetics. In his study, J. Timothy Greenamyre carries out multidisciplinary Genetics and Bioinformatics research.

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

Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines

Alexander V. Panov;Claire-Anne Gutekunst;Blair R. Leavitt;Michael R. Hayden.
Nature Neuroscience (2002)

1180 Citations

Mechanism of toxicity in rotenone models of Parkinson's disease.

Todd B. Sherer;Ranjita Betarbet;Claudia M. Testa;Byoung Boo Seo.
The Journal of Neuroscience (2003)

1100 Citations

Subcutaneous Rotenone Exposure Causes Highly Selective Dopaminergic Degeneration and α-Synuclein Aggregation

Todd B Sherer;Jin Ho Kim;Jin Ho Kim;Ranjita Betarbet;J Timothy Greenamyre.
Experimental Neurology (2003)

925 Citations

Animal models of Parkinson's disease

Ranjita Betarbet;Todd B. Sherer;J. Timothy Greenamyre.
BioEssays (2002)

758 Citations

A highly reproducible rotenone model of Parkinson's disease

Jason R. Cannon;Victor M. Tapias;Hye Mee Na;Anthony S. Honick.
Neurobiology of Disease (2009)

716 Citations

An In Vitro Model of Parkinson's Disease: Linking Mitochondrial Impairment to Altered α-Synuclein Metabolism and Oxidative Damage

Todd B. Sherer;Ranjita Betarbet;Amy K. Stout;Serena Lund.
The Journal of Neuroscience (2002)

704 Citations

Excitatory amino acids and Alzheimer's disease.

J.Timothy Greenamyre;Anne B. Young.
Neurobiology of Aging (1989)

643 Citations

Parkinson's--Divergent Causes, Convergent Mechanisms

J. Timothy Greenamyre;Teresa G. Hastings.
Science (2004)

533 Citations

Increased apoptosis of Huntington disease lymphoblasts associated with repeat length-dependent mitochondrial depolarization

Akira Sawa;Gordon W. Wiegand;Jillian Cooper;Russell L. Margolis.
Nature Medicine (1999)

508 Citations

N-Terminal Mutant Huntingtin Associates with Mitochondria and Impairs Mitochondrial Trafficking

Adam L. Orr;Shihua Li;Chuan-En Wang;He Li.
The Journal of Neuroscience (2008)

445 Citations

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