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Mikhail B. Bogdanov

Researcher at Cornell University

Publications -  25
Citations -  5147

Mikhail B. Bogdanov is an academic researcher from Cornell University. The author has contributed to research in topics: In vivo & Oxidative stress. The author has an hindex of 21, co-authored 25 publications receiving 4961 citations. Previous affiliations of Mikhail B. Bogdanov include Harvard University & United States Department of Veterans Affairs.

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Mice Deficient in Cellular Glutathione Peroxidase Show Increased Vulnerability to Malonate, 3-Nitropropionic Acid, and 1-Methyl-4-Phenyl-1,2,5,6-Tetrahydropyridine

TL;DR: The present results indicate that a knock-out of GSHPx may be adequately compensated under nonstressed conditions, but that after administration of mitochondrial toxins GSHpx plays an important role in detoxifying increases in oxygen radicals.
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Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis

TL;DR: It was found that oral administration of creatine produced a dose-dependent improvement in motor performance and extended survival in G93A transgenic mice, and it protected mice from loss of both motor neurons and substantia nigra neurons at 120 days of age.
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Mutant LRRK2R1441G BAC transgenic mice recapitulate cardinal features of Parkinson’s disease

TL;DR: A LRRK2 transgenic mouse model is created that recapitulates cardinal features of Parkinson's disease: an age-dependent and levodopa-responsive slowness of movement associated with diminished dopamine release and axonal pathology of nigrostriatal dopaminergic projection.
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Metabolomic profiling to develop blood biomarkers for Parkinson's disease.

TL;DR: In this article, the authors used metabolomic profiling using high performance liquid chromatography coupled with electrochemical coulometric array detection (LCECA) to look for biomarkers in plasma useful for the diagnosis of Parkinson's disease.
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Urate as a predictor of the rate of clinical decline in Parkinson disease.

TL;DR: Higher serum and cerebrospinal fluid urate concentrations at baseline were associated with slower rates of clinical decline and the link between urate concentration and PD is strengthened and the rationale for considering central nervous system urATE concentration elevation as a potential strategy to slow PD progression is strengthened.