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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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Dietary factors, hormesis and health.

TL;DR: New findings suggest that several heavily studied phytochemicals exhibit biphasic dose responses on cells with low doses activating signaling pathways that result in increased expression of genes encoding cytoprotective proteins including antioxidant enzymes, protein chaperones, growth factors and mitochondrial proteins.
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A neural signaling triumvirate that influences ageing and age-related disease: insulin/IGF-1, BDNF and serotonin.

TL;DR: The ageing process and its associated diseases all involve perturbed energy metabolism, oxidative damage, and an impaired ability of the organism and its cells to cope with adversity, so it is proposed that some specific signaling pathways in the brain may be important determinants of health during ageing.
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Mitochondrial SIRT3 Mediates Adaptive Responses of Neurons to Exercise and Metabolic and Excitatory Challenges

TL;DR: It is shown that the mitochondrial protein deacetylase SIRT3 mediates adaptive responses of neurons to bioenergetic, oxidative, and excitatory stress and plays pivotal roles in adaptive responses to physiological challenges and resistance to degeneration.
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Exacerbation of Damage and Altered NF-κB Activation in Mice Lacking Tumor Necrosis Factor Receptors after Traumatic Brain Injury

TL;DR: Analysis of NF-κB activation and relative levels of MnSOD revealed delayed responses in the injured cortex of TNFR-KO animals compared with wild-type animals, implying that endogenous TNFα may be neuroprotective after TBI.
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Neuronal calcium homeostasis and dysregulation.

TL;DR: Advances in understanding the molecular regulation of Ca(2+) homeostasis and how it is perturbed in neurological disorders may lead to therapeutic strategies that modulate neuronal Ca( 2+) signaling to enhance function and counteract disease processes.