World's Best Scientists 2026 revealed!
James B. Koprich

James B. Koprich

D-Index & Metrics

Neuroscience

D-Index
37
Citations
4613
World Ranking
8853
National Ranking
137

Overview

James B. Koprich is affiliated with Fudan University in China and focuses their research primarily within the fields of Medicine and Neuroscience. Their work encompasses several subfields including Neurology, Cellular and Molecular Neuroscience, Molecular Biology, Epidemiology, and Cell Biology.

The main topics addressed in their research include:

  • Parkinson's Disease Mechanisms and Treatments
  • Neurological disorders and treatments
  • Nerve injury and regeneration
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Nuclear Receptors and Signaling
  • Cellular transport and secretion
  • RNA regulation and disease

James B. Koprich has published extensively, with notable recent papers as follows:

  • "Early-onset impairment of the ubiquitin-proteasome system in dopaminergic neurons caused by α-synuclein," 2020, Acta Neuropathologica Communications
  • "Neurodegeneration by α-synuclein-specific T cells in AAV-A53T-α-synuclein Parkinson's disease mice," 2022, Brain Behavior and Immunity
  • "The Promise and Challenges of Developing miRNA-Based Therapeutics for Parkinson's Disease," 2020, Cells
  • "Propagated α-synucleinopathy recapitulates REM sleep behaviour disorder followed by parkinsonian phenotypes in mice," 2020, Brain
  • "Neuroprotection of Exendin-4 by Enhanced Autophagy in a Parkinsonian Rat Model of α-Synucleinopathy," 2021, Neurotherapeutics

Their frequent co-authors include:

  • Jonathan M. Brotchie
  • Chi Wang Ip
  • Jens Volkmann
  • Rhonda L. McFleder
  • Thomas Musacchio

James B. Koprich's research contributions have been published predominantly in the following venues:

  • Brain Behavior and Immunity
  • Clinical Neurophysiology
  • Brain
  • Journal of Neuroinflammation
  • npj Parkinson s Disease

Best Publications

  • Dynamic Changes in Presynaptic and Axonal Transport Proteins Combined with Striatal Neuroinflammation Precede Dopaminergic Neuronal Loss in a Rat Model of AAV α-Synucleinopathy

    Chee Yeun Chung;James B. Koprich;Hasan Siddiqi;Ole Isacson

  • Neuroinflammation mediated by IL-1β increases susceptibility of dopamine neurons to degeneration in an animal model of Parkinson's disease

    James B Koprich;Casper Reske-Nielsen;Prabhakar Mithal;Ole Stefan Isacson

  • The Pharmacology of l-DOPA-Induced Dyskinesia in Parkinson’s Disease

    Philippe Huot;Tom H. Johnston;James B. Koprich;Susan H. Fox

  • Animal models of α-synucleinopathy for Parkinson disease drug development

    James B. Koprich;Lorraine V. Kalia;Jonathan M. Brotchie

  • AAV1/2-induced overexpression of A53T-α-synuclein in the substantia nigra results in degeneration of the nigrostriatal system with Lewy-like pathology and motor impairment: a new mouse model for Parkinson’s disease

    Chi Wang Ip;Laura-Christin Klaus;Akua A. Karikari;Naomi P. Visanji

  • Expression of human A53T alpha-synuclein in the rat substantia nigra using a novel AAV1/2 vector produces a rapidly evolving pathology with protein aggregation, dystrophic neurite architecture and nigrostriatal degeneration with potential to model the pathology of Parkinson's disease

    James B Koprich;Tom H Johnston;M Gabriela Reyes;Xuan Sun

  • α-Synuclein-Based Animal Models of Parkinson's Disease: Challenges and Opportunities in a New Era

    Naomi P. Visanji;Jonathan M. Brotchie;Lorraine V. Kalia;James B. Koprich

  • Treatment with Trehalose Prevents Behavioral and Neurochemical Deficits Produced in an AAV α-Synuclein Rat Model of Parkinson’s Disease

    Qing He;Qing He;James B. Koprich;Ying Wang;Wen-bo Yu

  • Neurodegeneration by α-synuclein-specific T cells in AAV-A53T-α-synuclein Parkinson’s disease mice

    Unknown

  • Early-onset impairment of the ubiquitin-proteasome system in dopaminergic neurons caused by α-synuclein

    Chris McKinnon;Mitchell L. De Snoo;Elise Gondard;Clemens Neudorfer

  • The Toll-Like Receptor-3 Agonist Polyinosinic:Polycytidylic Acid Triggers Nigrostriatal Dopaminergic Degeneration

    Michela Deleidi;Penelope J. Hallett;James B. Koprich;Chee-Yeun Chung

  • Progressive neurodegeneration or endogenous compensation in an animal model of Parkinson's disease produced by decreasing doses of alpha-synuclein.

    James B. Koprich;Tom H. Johnston;Philippe Huot;M. Gabriela Reyes

  • Characterization of 3,4-methylenedioxymethamphetamine (MDMA) enantiomers in vitro and in the MPTP-lesioned primate: R-MDMA reduces severity of dyskinesia, whereas S-MDMA extends duration of ON-time.

    P. Huot;T.H. Johnston;Katie Lewis;J.B. Koprich

  • Subthalamic nucleus deep brain stimulation is neuroprotective in the A53T α‐synuclein Parkinson's disease rat model

    Thomas Musacchio;Maike Rebenstorff;Felix Fluri;Jonathan M. Brotchie

  • Nigrostriatal Dysfunction in Familial Alzheimer's Disease-Linked APPswe/PS1ΔE9 Transgenic Mice

    Sylvia E. Perez;Orly Lazarov;James B. Koprich;Er Yun Chen

  • The selective mu-opioid receptor antagonist ADL5510 reduces levodopa-induced dyskinesia without affecting antiparkinsonian action in MPTP-lesioned macaque model of Parkinson's disease.

    James B. Koprich;Susan H. Fox;Tom H. Johnston;Allan Goodman

  • Prenatal 3,4-methylenedioxymethamphetamine (ecstasy) alters exploratory behavior, reduces monoamine metabolism, and increases forebrain tyrosine hydroxylase fiber density of juvenile rats.

    James B. Koprich;Er Yun Chen;Nicholas M. Kanaan;Nicholas G. Campbell

  • Neonatal 3,4-methylenedioxymethamphetamine (ecstasy) alters dopamine and serotonin neurochemistry and increases brain-derived neurotrophic factor in the forebrain and brainstem of the rat.

    James B Koprich;Nicholas G Campbell;Jack W Lipton

  • Propagated α-synucleinopathy recapitulates REM sleep behaviour disorder followed by parkinsonian phenotypes in mice.

    Yan Shen;Wen-Bo Yu;Bo Shen;Hui Dong

  • The Promise and Challenges of Developing miRNA-Based Therapeutics for Parkinson's Disease.

    Simoneide S. Titze-de-Almeida;Cristina Soto-Sánchez;Eduardo Fernandez;James B. Koprich

  • UWA-121, a mixed dopamine and serotonin re-uptake inhibitor, enhances L-DOPA anti-parkinsonian action without worsening dyskinesia or psychosis-like behaviours in the MPTP-lesioned common marmoset.

    Philippe Huot;Tom H. Johnston;Katie D. Lewis;James B. Koprich

  • A53T-α-synuclein overexpression in murine locus coeruleus induces Parkinson’s disease-like pathology in neurons and glia

    Martin Timo Henrich;Fanni Fruzsina Geibl;Bolam Lee;Wei-Hua Chiu

  • Response of aged parkinsonian monkeys to in vivo gene transfer of GDNF.

    M.E. Emborg;J. Moirano;J. Raschke;V. Bondarenko

Frequent Co-Authors

Jack W. Lipton
Jack W. Lipton Michigan State University
Ole Isacson
Ole Isacson Harvard University
Menachem Hanani
Menachem Hanani Hebrew University of Jerusalem
Jeffrey H. Kordower
Jeffrey H. Kordower Arizona State University
Sylvia E. Perez
Sylvia E. Perez Barrow Neurological Institute
Elliott J. Mufson
Elliott J. Mufson Barrow Neurological Institute
Nicholas M. Kanaan
Nicholas M. Kanaan Michigan State University
Penelope J. Hallett
Penelope J. Hallett Harvard University
James H. Eubanks
James H. Eubanks University Health Network
Jacqueline N. Crawley
Jacqueline N. Crawley University of California, Davis

If you think any of the details on this page are incorrect, let us know.

Report an issue

We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below:

Related Online Degrees & Career Pathways

Pursuing a neuroscience degree in the USA opens up a variety of avenues, both on-campus and online. Many students are choosing flexible learning options, such as online degree programs, to accommodate work or family commitments.

For those mindful of tuition costs, exploring online colleges that accept fafsa can provide access to financial aid and affordable tuition, making higher education more accessible.

While neuroscience is intellectually rewarding, some students may want to compare the field’s earning potential with which degrees make the most money. This can help guide decisions about whether to pursue neuroscience or a related, high-demand major.

Additionally, supplementing your degree with specialized credentials can boost career prospects. Explore online certifications that pay well to expand your skills in fields like data analysis, programming, or healthcare management, complementing your neuroscience background.

Best Scientists Citing James B. Koprich

Trending Scientists

Recently Published Articles