M
Mahmoud Kiaei
Researcher at University of Arkansas for Medical Sciences
Publications - 54
Citations - 4484
Mahmoud Kiaei is an academic researcher from University of Arkansas for Medical Sciences. The author has contributed to research in topics: Amyotrophic lateral sclerosis & SOD1. The author has an hindex of 34, co-authored 50 publications receiving 4064 citations. Previous affiliations of Mahmoud Kiaei include Cornell University & Icahn School of Medicine at Mount Sinai.
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Journal ArticleDOI
Mutated human SOD1 causes dysfunction of oxidative phosphorylation in mitochondria of transgenic mice.
Marina Mattiazzi,Marilena D'Aurelio,Carl D. Gajewski,Katherine Martushova,Mahmoud Kiaei,M. Flint Beal,Giovanni Manfredi +6 more
TL;DR: The findings suggest that G93A-mutated hSOD1 in mitochondria may cause mitochondrial defects, which contribute to precipitating the neurodegenerative process in motor neurons.
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Neural mitochondrial Ca2+ capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn-superoxide dismutase mutant mice.
Maria Damiano,Anatoly A. Starkov,Susanne Petri,Kathuna Kipiani,Mahmoud Kiaei,Marina Mattiazzi,M. Flint Beal,Giovanni Manfredi +7 more
TL;DR: Mitochondrial dysfunction and Ca2+‐mediated excitotoxicity are likely to be interconnected mechanisms that contribute to neuronal degeneration in familial amyotrophic lateral sclerosis.
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Impaired PGC-1α function in muscle in Huntington's disease
Rajnish Kumar Chaturvedi,Peter J. Adhihetty,S. Shukla,Thomas Hennessy,Noel Y. Calingasan,Lichuan Yang,Anatoly A. Starkov,Mahmoud Kiaei,Milena Cannella,Jenny Sassone,Andrea Ciammola,Fernando Squitieri,M. Flint Beal +12 more
TL;DR: Findings show that impaired function of PGC-1alpha plays a critical role in muscle dysfunction in Huntington's disease, and that treatment with agents to enhance P GC-1 alpha function could exert therapeutic benefits, and muscle may provide a readily accessible tissue in which to monitor therapeutic interventions.
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Peroxisome proliferator-activated receptor-gamma agonist extends survival in transgenic mouse model of amyotrophic lateral sclerosis
TL;DR: Investigation of the therapeutic effect of pioglitazone in the G93A SOD1 transgenic mouse model of ALS suggests that the drug may have therapeutic potential for human ALS.
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Additive neuroprotective effects of creatine and cyclooxygenase 2 inhibitors in a transgenic mouse model of amyotrophic lateral sclerosis.
TL;DR: The results suggest that combinations of therapies targeting different disease mechanisms may be a useful strategy in the treatment of ALS.