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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Secreted forms of β‐amyloid precursor protein modulate dendrite outgrowth and calcium responses to glutamate in cultured embryonic hippocampal neurons
TL;DR: Secreted forms of the beta-amyloid precursor protein (APPss) counteracted the inhibitory effect of glutamate on dendrite outgrowth in cultured embryonic hippocampal neurons and may play a role in developmental and synaptic plasticity by modulating dendritic responses to glutamate.
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Impact of lysosome status on extracellular vesicle content and release.
TL;DR: A better understanding of the molecular mechanisms that regulate trafficking of MVBs to lysosomes and the plasma membrane may advance an understanding of diseases in which pathogenic proteins, lipids or infectious agents accumulate within or outside of cells.
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3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons
Krisztina Marosi,Sang Woo Kim,Keelin Moehl,Morten Scheibye-Knudsen,Aiwu Cheng,Roy G. Cutler,Simonetta Camandola,Mark P. Mattson,Mark P. Mattson +8 more
TL;DR: It is found that 3OHB metabolism increases mitochondrial respiration which drives changes in expression of brain‐derived neurotrophic factor (BDNF) in cultured cerebral cortical neurons.
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Role of Cyclic GMP in the Regulation of Neuronal Calcium and Survival by Secreted Forms of β‐Amyloid Precursor
TL;DR: Data suggest that APPss mediate their [Ca2+]i‐lowering and excitoprotective effects on target neurons through increases in cGMP levels.
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Altered calcium homeostasis and mitochondrial dysfunction in cortical synaptic compartments of presenilin-1 mutant mice.
TL;DR: It is reported that synaptosomes prepared from transgenic mice harboring presenilin‐1 mutations exhibit enhanced elevations of cytoplasmic calcium levels following exposure to depolarizing agents, amyloid β‐peptide, and a mitochondrial toxin compared with synaptoomes from nontransgenic mice and mice overexpressing wild‐type presenILin‐ 1.