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Amit K. Chouhan
Researcher at University of St Andrews
Publications - 11
Citations - 685
Amit K. Chouhan is an academic researcher from University of St Andrews. The author has contributed to research in topics: Motor neuron & Erg. The author has an hindex of 11, co-authored 11 publications receiving 526 citations. Previous affiliations of Amit K. Chouhan include University of Texas Southwestern Medical Center & University of Texas Health Science Center at San Antonio.
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Journal ArticleDOI
C9ORF72 repeat expansion causes vulnerability of motor neurons to Ca2+-permeable AMPA receptor-mediated excitotoxicity
Bhuvaneish T. Selvaraj,Matthew R. Livesey,Chen Zhao,Jenna M. Gregory,Owain T. James,Elaine M. Cleary,Amit K. Chouhan,Amit K. Chouhan,Angus B. Gane,Emma M. Perkins,Owen Dando,Simon G. Lillico,Youn-Bok Lee,Agnes L. Nishimura,Urjana Poreci,Sai Thankamony,Meryll Pray,Navneet A. Vasistha,Dario Magnani,Shyamanga Borooah,Karen Burr,David Story,Alexander McCampbell,Christopher Shaw,Peter C. Kind,Timothy J. Aitman,C. Bruce A. Whitelaw,Ian Wilmut,Colin Smith,Gareth B. Miles,Gareth B. Miles,Giles E. Hardingham,David J. A. Wyllie,Siddharthan Chandran +33 more
TL;DR: It is shown that increased expression of GluA1 AMPA receptor (AMPAR) subunit occurs in MNs with C9ORF72 mutations that leads to increased Ca2+-permeable AMPAR expression and results in enhanced selective MN vulnerability to excitotoxicity.
Journal ArticleDOI
Discovery and functional prioritization of Parkinson's disease candidate genes from large-scale whole exome sequencing
Iris E. Jansen,Iris E. Jansen,Hui Ye,Sasja Heetveld,Marie C. Lechler,Helen Michels,Renée I. Seinstra,Steven J. Lubbe,Steven J. Lubbe,Valérie Drouet,Suzanne Lesage,Elisa Majounie,J. Raphael Gibbs,Mike A. Nalls,Mina Ryten,Mina Ryten,Juan A. Botía,Jana Vandrovcova,Javier Simón-Sánchez,Javier Simón-Sánchez,Melissa Castillo-Lizardo,Patrizia Rizzu,Cornelis Blauwendraat,Amit K. Chouhan,Yarong Li,Puja Yogi,Najaf Amin,Cornelia M. van Duijn,Huw R. Morris,Alexis Brice,Andrew B. Singleton,Della C. David,Ellen A. A. Nollen,Shushant Jain,Joshua M. Shulman,Peter Heutink,Peter Heutink,Peter Heutink +37 more
TL;DR: By integrating human genetic and functional evidence, this work identifies several PD susceptibility gene candidates for further investigation and highlights a powerful experimental strategy with broad applicability for future studies of disorders with complex genetic etiologies.
Journal ArticleDOI
Uncoupling neuronal death and dysfunction in Drosophila models of neurodegenerative disease
Amit K. Chouhan,Caiwei Guo,Yi-Chen Hsieh,Hui Ye,Mumine Senturk,Zhongyuan Zuo,Yarong Li,Shreyasi Chatterjee,Juan Botas,George R. Jackson,George R. Jackson,George R. Jackson,Hugo J. Bellen,Joshua M. Shulman +13 more
TL;DR: Interestingly, Tau and αSyn each cause prominent but distinct synaptotoxic profiles, including disorganization or enlargement of photoreceptor terminals, respectively, which highlight variable and dynamic properties of neurodegeneration triggered by these disease-relevant proteins in vivo.
Journal ArticleDOI
Presynaptic Mitochondria in Functionally Different Motor Neurons Exhibit Similar Affinities for Ca2+ But Exert Little Influence as Ca2+ Buffers at Nerve Firing Rates In Situ
TL;DR: Findings indicate that presynaptic mitochondria have a similar affinity for Ca2+ in functionally different nerve terminals, but do not limit cytosolicCa2+ levels within the range of motor neuron firing rates in situ.
Journal ArticleDOI
Mutant C9orf72 human iPSC-derived astrocytes cause non-cell autonomous motor neuron pathophysiology.
Chen Zhao,Anna-Claire Devlin,Anna-Claire Devlin,Amit K. Chouhan,Amit K. Chouhan,Bhuvaneish T. Selvaraj,Maria Stavrou,Karen Burr,Veronica Brivio,Veronica Brivio,Xin He,Arpan R Mehta,David Story,Christopher Shaw,Owen Dando,Giles E. Hardingham,Gareth B. Miles,Gareth B. Miles,Siddharthan Chandran +18 more
TL;DR: It is shown that mutant astrocytes both recapitulate key aspects of C9orf72‐related ALS pathology and, upon co‐culture, cause motor neurons to undergo a progressive loss of action potential output due to decreases in the magnitude of voltage‐activated Na+ and K+ currents.