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
Neurodegeneration: nicked to death.
David M. Wilson,Mark P. Mattson +1 more
TL;DR: A recent study demonstrates that aprataxin is critical for the processing of obstructive DNA termini, suggesting a broader role for DNA single-strand break repair in neurodegenerative disease.
Book
Stem Cells: A Cellular Fountain of Youth
Mark P. Mattson,Gary Van Zant +1 more
TL;DR: This work focuses on the development and differentiation of Myogenic Stem Cells in Skeletal Muscle Growth and Regeneration, as well as myocardial Aging and Embryonic Stem Cell Biology.
Journal ArticleDOI
Nitro-PDI incites toxic waste accumulation.
TL;DR: In Parkinson disease and related disorders, nitric oxide may disable PDI, an enzyme critical for proper protein folding in the endoplasmic reticulum, resulting in the accumulation of damaged proteins and eventually neuronal death.
Journal ArticleDOI
Acetylation Unleashes Protein Demons of Dementia
TL;DR: It is shown that acetylation of the amino acid lysine in the microtubule-associated protein tau prevents its ubiquitin-mediated degradation, resulting in "tau tangles" similar to those of dementias.
Journal ArticleDOI
Postnatal TLR2 activation impairs learning and memory in adulthood
Ravit Madar,Aviva Rotter,Hiba Waldman Ben-Asher,Mohamed R. Mughal,Thiruma V. Arumugam,William H. Wood,Kevin G. Becker,Mark P. Mattson,Eitan Okun +8 more
TL;DR: The data indicate that postnatal TLR2 activation affects learning and memory in adult mice in a heterodimer-dependent manner, and implies that adult cognitive behavior could be influenced in part, by activation or alterations in theTLR2 pathway at birth.