M
Mark P. Mattson
Researcher at Johns Hopkins University School of Medicine
Publications - 988
Citations - 151506
Mark P. Mattson is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Glutamate receptor & Neuroprotection. The author has an hindex of 200, co-authored 980 publications receiving 138033 citations. Previous affiliations of Mark P. Mattson include University of Kentucky & National Institutes of Health.
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NT-3 and BDNF protect CNS neurons against metabolic/excitotoxic insults.
Bin Cheng,Mark P. Mattson +1 more
TL;DR: The data demonstrate that NT-3 and BDNF can protect neurons against metabolic and excitotoxic insults, and suggest that these neurotrophins may serve [Ca2+]i-stabilizing and neuroprotective functions in the brain.
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β-Amyloid Peptide Free Radical Fragments Initiate Synaptosomal Lipoperoxidation in a Sequence-Specific Fashion: Implications to Alzheimer′s Disease
TL;DR: It is reported that Aβ(25-35) is a potent lipoperoxidation initiator, as inferred from peptide-mediated reduction of nitroxyl stearate spin labels bound to rodent neocortical synaptosomal membranes, a "molecular shrapnel" model of neuronal membrane damage in Alzheimer′s disease.
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Food restriction reduces brain damage and improves behavioral outcome following excitotoxic and metabolic insults.
TL;DR: FR greatly increased the resistance of rats to kainate‐induced deficits in performance in water‐maze learning and memory tasks, and to 3‐nitropropionic acid–induced impairment of motor function, suggesting that FR not only extends life span, but increases resistance of the brain to insults that involve metabolic compromise and excitotoxicity.
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Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice
Wenzhen Duan,Zhihong Guo,Haiyang Jiang,Melvin Ware,Xiao-Jiang Li,Mark P. Mattson,Mark P. Mattson +6 more
TL;DR: The suppression of the pathogenic processes by DR in HD mice suggests that mutant huntingtin promotes neuronal degeneration by impairing cellular stress resistance, and that the body wasting in HD is driven by the neurodegenerative process.
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Brain metabolism in health, aging, and neurodegeneration
TL;DR: It is suggested that lifestyles that include intermittent bioenergetic challenges, most notably exercise and dietary energy restriction, can increase the likelihood that the brain will function optimally and in the absence of disease throughout life.