scispace - formally typeset
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.

Papers
More filters
Journal ArticleDOI

Partial loss of the DNA repair scaffolding protein, Xrcc1, results in increased brain damage and reduced recovery from ischemic stroke in mice.

TL;DR: Impaired BER is a risk factor in ischemic brain injury and contributes to its recovery, and significant losses of thymine glycol incision, abasic endonucleaseincision, and single nucleotide incorporation activities were identified.
Patent

Cytochalasins useful in providing protection against nerve cell injury associated with neurodegenerative disorders

TL;DR: In this paper, the authors proposed novel therapeutic uses of certain compounds to protect nerve cells from injury and death, including cytochalasin D and related analogs, and cyto-chalasin E and its analogs.
Journal ArticleDOI

Age-associated alterations in the levels of cytotoxic lipid molecular species and oxidative stress in the murine thymus are reduced by growth hormone treatment.

TL;DR: There is a correlation between reduced thymocyte numbers and markers of inflammation and oxidative stress with age and growth hormone treatment attenuated inflammation and age-related increases in oxidative stress and lipotoxicity in the thymus.
Journal ArticleDOI

Amyloid β-peptide alters thrombin-induced calcium responses in cultured human neural cells

TL;DR: It is shown that human SH-SY5Y neuroblastoma cells expressed thrombin receptors linked to Ca2+ release from intracellular stores that are linked to inositol phospholipid hydrolysis and elevation of [Ca2+]i.
Journal ArticleDOI

Mice lacking the transcriptional regulator Bhlhe40 have enhanced neuronal excitability and impaired synaptic plasticity in the hippocampus.

TL;DR: A role for Bhlhe40 in regulating neuronal excitability and synaptic plasticity in the hippocampus is supported and indirect regulation of Ide transcription may be involved in these phenotypes.