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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How does the brain control lifespan
TL;DR: It is speculated that during evolution the brain took on the task of monitoring and controlling peripheral energy metabolism, and thereby regulating lifespan in the context of food availability, suggesting a mechanism whereby the brain can control lifespan.
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The Microenvironment of the Embryonic Neural Stem Cell: Lessons From Adult Niches?
Justin D. Lathia,Justin D. Lathia,Mahendra S. Rao,Mahendra S. Rao,Mark P. Mattson,Charles ffrench-Constant +5 more
TL;DR: Using the similarities and differences observed, it will be considered whether the location of embryonic stem cell populations such as the VZ can be thought of as niches and how these lessons from the niche inform the understanding of neurodevelopmental diseases and cancers of the CNS.
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Cockayne syndrome group A and B proteins converge on transcription-linked resolution of non-B DNA.
Morten Scheibye-Knudsen,Morten Scheibye-Knudsen,Anne Tseng,Martin Borch Jensen,Karsten Scheibye-Alsing,Evandro Fei Fang,Teruaki Iyama,Sanjay Kumar Bharti,Krisztina Marosi,Lynn Froetscher,Henok Kassahun,David Mark Eckley,Robert W. Maul,Paul Bastian,Supriyo De,Soumita Ghosh,Hilde Nilsen,Ilya G. Goldberg,Mark P. Mattson,David M. Wilson,Robert M. Brosh,Myriam Gorospe,Vilhelm A. Bohr +22 more
TL;DR: Evidence is presented that loss of CSA or CSB in a neuroblastoma cell line converges on mitochondrial dysfunction caused by defects in ribosomal DNA transcription and activation of the DNA damage sensor poly-ADP ribose polymerase 1 (PARP1).
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Presenilin-1 mutation sensitizes oligodendrocytes to glutamate and amyloid toxicities, and exacerbates white matter damage and memory impairment in mice.
TL;DR: Oligodendrocytes from PS1 mutant knockin mice are more vulnerable to being killed by glutamate and amyloid β-peptide, and exhibit an abnormality in calcium regulation which is responsible for their death.