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
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Journal ArticleDOI
No more brain tangles with ΔNp73
Mark P. Mattson,Uri Ashery +1 more
TL;DR: Findings provide a novel animal model of AD and a potential therapeutic role for DeltaNp73 inducers and a surprising neuroprotective role for a truncated p73 isoform (DeltaNp 73).
Journal ArticleDOI
Defects of immune regulation in the presenilin-1 mutant knockin mouse.
Grant Morgan,Qing Guo,Sic L. Chan,Devin S. Gary,Barbara A. Osborne,Mark P. Mattson,Mark P. Mattson +6 more
TL;DR: It is reported that splenocytes from PS1-mutant (M146V) knockin mice exhibit increased caspase activity, abnormal calcium regulation and aberrant mitochondrial function, which suggests that abnormalities in immune function might play major roles in the pathogenesis of AD.
Journal ArticleDOI
An ECSIT‐centric view of Alzheimer's disease (Comment on DOI 10.1002/bies.201100193)
TL;DR: A role for a protein called ECSIT, believed to function in the integration of cellular stress responses, as a key node in the signaling networks gone awry in AD is proposed, providing a framework for future studies to test the authors’ hypothesis.
Book ChapterDOI
Sphingomyelin and ceramide in brain aging, neuronal plasticity and neurodegenerative disorders
TL;DR: The emerging evidence suggesting that sphingomyelin alterations play important roles in dysfunction and death of neurons in pathological conditions and that normalizing these alterations may prove effective in preventing and treating one or more of the diseases is reviewed.
Book ChapterDOI
The Fundamental Role of Hormesis in Evolution
TL;DR: Examples of environmental conditions that can, at subtoxic levels, activate hormetic responses and examples of the genes and cellular and molecular pathways that mediate such adaptive stress responses are provided to illustrate how hormesis mediates natural selection.