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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Cell-extracellular matrix interactions regulate neural differentiation of human embryonic stem cells
TL;DR: Laminin is defined as a key ECM molecule to enhance neural progenitor generation, expansion and differentiation into neurons from hESCs and the cell-laminin interactions involve α6β1 integrin receptors implicating a possible role of laminin/α6β 1 integrin signaling in directed neural differentiation of hESC.
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HIV-1 Tat through phosphorylation of NMDA receptors potentiates glutamate excitotoxicity.
Norman J. Haughey,Norman J. Haughey,Avi Nath,Mark P. Mattson,John T. Slevin,Jonathan D. Geiger +5 more
TL;DR: It is suggested that NMDA receptors play an important role in Tat neurotoxicity and the mechanisms identified may provide additional therapeutic targets for the treatment of HIV‐1 associated dementia.
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Presenilins, the Endoplasmic Reticulum, and Neuronal Apoptosis in Alzheimer's Disease
TL;DR: When expressed in cultured cells and transgenic mice, mutant PSs promote increased production of a long form of amyloid β‐peptide (Aβ1‐42) that may possess enhancedAmyloidogenic and neurotoxic properties.
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Nicotinamide prevents NAD+ depletion and protects neurons against excitotoxicity and cerebral ischemia: NAD+ consumption by SIRT1 may endanger energetically compromised neurons.
TL;DR: SIRT1 is linked to bioenergetic state and stress responses in neurons, and that under conditions of reduced cellular energy levels SIRT1 enzyme activity may consume sufficient NAD+ to nullify any cell survival-promoting effects of its deacetylase action on protein substrates.
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Cellular signaling roles of TGFβ, TNFα and βAPP in brain injury responses and Alzheimer's disease
Mark P. Mattson,Steven W. Barger,Katsutoshi Furukawa,Annadora J. Bruce,Tony Wyss-Coray,Robert J. Mark,Lennart Mucke +6 more
TL;DR: For example, the authors showed that TGF beta, TNF alpha and the fibrillogenic amyloid beta-peptide (A beta) derivative of beta APP can promote damage of neuronal and glial cells, and may play roles in neurodegenerative disorders.