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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Presenilin-1 Mutation Increases Neuronal Vulnerability to Focal Ischemia In Vivo and to Hypoxia and Glucose Deprivation in Cell Culture: Involvement of Perturbed Calcium Homeostasis
TL;DR: The data suggest that presenilin mutations may promote neuronal degeneration in AD by increasing the sensitivity of neurons to age-related ischemia-like conditions, and drugs that stabilize endoplasmic reticulum calcium homeostasis may prove effective in suppressing the neurodegenerative process in AD patients.
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Toll-Like Receptor 3 Is a Negative Regulator of Embryonic Neural Progenitor Cell Proliferation
Justin D. Lathia,Eitan Okun,Sung-Chun Tang,Kathleen J. Griffioen,Aiwu Cheng,Mohamed R. Mughal,Gloria Laryea,Pradeep K. Selvaraj,Charles ffrench-Constant,Tim Magnus,Thiruma V. Arumugam,Mark P. Mattson +11 more
TL;DR: A novel role for TLR3 is revealed in the negative regulation of NPC proliferation in the developing brain in wild type but notTLR3−/−-derived NPCs.
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The Catalytic Subunit of Telomerase Protects Neurons Against Amyloid β‐Peptide‐Induced Apoptosis
TL;DR: The catalytic subunit of telomerase (TERT) is a specialized reverse transcriptase that has been associated with cell immortalization and cancer as mentioned in this paper, and suppression of TERT levels and function in embryonic mouse hippocampal neurons in culture using antisense technology and the Telomerase inhibitor 3' -azido-2' 3'dideoxythymidine significantly increases their vulnerability to cell death induced by amyloid beta-peptide, a neurotoxic protein believed to promote neuronal degeneration in Alzheimer's disease.
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Posteromedial cortex glutamate and GABA predict intrinsic functional connectivity of the default mode network
TL;DR: It is concluded that regional neurotransmitter concentrations in a network node strongly predict network but not global brain iFC.
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Exendin-4 Improves Glycemic Control, Ameliorates Brain and Pancreatic Pathologies, and Extends Survival in a Mouse Model of Huntington's Disease
Bronwen Martin,Erin Golden,Olga D. Carlson,Paul J. Pistell,Jie Zhou,Wook Kim,Brittany P. Frank,Sam Thomas,Wayne Chadwick,Nigel H. Greig,Gillian P. Bates,Kirupa Sathasivam,Michel Bernier,Stuart Maudsley,Mark P. Mattson,Josephine M. Egan +15 more
TL;DR: Targeting both peripheral and neuronal deficits, Ex-4 is an attractive agent for therapeutic intervention in Huntington's disease patients suffering from diabetes.