scispace - formally typeset
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.

Papers
More filters
Journal ArticleDOI

Mutated human SOD1 causes dysfunction of oxidative phosphorylation in mitochondria of transgenic mice.

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.
Journal ArticleDOI

Neural mitochondrial Ca2+ capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn-superoxide dismutase mutant mice.

TL;DR: Mitochondrial dysfunction and Ca2+‐mediated excitotoxicity are likely to be interconnected mechanisms that contribute to neuronal degeneration in familial amyotrophic lateral sclerosis.
Journal ArticleDOI

Impaired PGC-1α function in muscle in Huntington's disease

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.