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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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A link between maze learning and hippocampal expression of neuroleukin and its receptor gp78

TL;DR: Interaction of NLK with gp78 and subsequent signaling may strengthen synaptic mechanisms underlying learning and memory formation, and application of recombinant NLK to hippocampal neurons significantly enhanced glutamate‐induced ion currents, functional molecular changes that have been correlated with learning in vivo.
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Biological sex and DNA repair deficiency drive Alzheimer's disease via systemic metabolic remodeling and brain mitochondrial dysfunction.

TL;DR: Novel mechanisms of glycolysis inhibition, PPP, and tricarboxylic acid cycle impairment, and a neuroprotective augmentation of lipid metabolism in AD are identified, which support a sex-targeted metabolism-modifying strategy to prevent and treat AD.
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The astrocytic transporter SLC7A10 (Asc-1) mediates glycinergic inhibition of spinal cord motor neurons.

TL;DR: These observations establish the etiology of sustained myoclonus (sudden involuntary muscle movements) and early postnatal lethality characteristic of Slc7a10-null mice, and implicate SLC7A10 as a candidate gene and auto-antibody target in human hyperekplexia and stiff person syndrome, respectively.
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Folate and Homocysteine Metabolism: Therapeutic Targets in Cardiovascular and Neurodegenerative Disorders

TL;DR: Dietary folate stimulates homocysteine removal and may thereby protect cells against disease processes and provide novel targets for drug discovery.
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Lowering corticosterone levels reinstates hippocampal brain-derived neurotropic factor and trkb expression without influencing deficits in hypothalamic brain-derived neurotropic factor expression in leptin receptor-deficient mice

TL;DR: In this paper, the expression of BDNF, its receptor TrkB, and neurotropin-3 (NT-3) was measured in the hippocampus and hypothalamus of leptin receptor-deficient mice and wild-type controls following low-dose corticosterone replacement (ADX+CORT) or sham operation.