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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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Amyloid β-peptide induces apoptosis-related events in synapses and dendrites

TL;DR: It is demonstrated that apoptotic biochemical cascades can be activated in synapses and dendrites by Aβ, and suggested that such `synaptic apoptosis' may contribute to synaptic dysfunction and degeneration in AD.
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The actin-severing protein gelsolin modulates calcium channel and NMDA receptor activities and vulnerability to excitotoxicity in hippocampal neurons.

TL;DR: Roles for gelsolin and the actin cytoskeleton are identified in controlling actin-mediated feedback regulation of Ca2+ influx and in neuronal injury responses and are suggested in both physiological and pathophysiological events that involve activation of NMDA receptors and VDCC.
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IGF-I and IGF-II protect cultured hippocampal and septal neurons against calcium-mediated hypoglycemic damage.

TL;DR: Findings indicate that IGFs can stabilize neuronal calcium homeostasis and thereby protect against hypoglycemic damage.
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A ketone ester diet exhibits anxiolytic and cognition-sparing properties, and lessens amyloid and tau pathologies in a mouse model of Alzheimer's disease

TL;DR: A novel ketone ester can ameliorate proteopathic and behavioral deficits in a mouse AD model by reducing levels of hyperphosphorylated tau deposition in the regions of the hippocampus, amygdala, and cortex.
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Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders.

TL;DR: The recent development of low molecular weight molecules that scavenge HNE suggests that HNE can be targeted in the design of drugs for the treatment of obesity, the metabolic syndrome, and associated disorders.