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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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TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration

TL;DR: It is found that TREM2 deficiency impaired microglia phagocytic clearance of pathological TDP-43, and enhanced neuronal damage and motor function impairments, and TAR-DNA binding protein 43 kDa (TDP- 43)-related neurodegenerative disease via viral-mediated expression of human TDP -43 protein in mice or inducible expression of hTDP43 with defective nuclear localization signals in transgenic mice.
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Sonic hedgehog expression in the postnatal brain

TL;DR: It is found that while the amounts of Shh transcript and protein in rat brains are nearly undetectable at birth, they increase continuously during postnatal development and remain at readily detectable levels in young adults.
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Seizures and tissue injury induce telomerase in hippocampal microglial cells

TL;DR: It is reported that telomerase activity and expression of TERT are induced in the hippocampus of adult mice after administration of the seizure-inducing excitotoxin kainate, and the first evidence that TERT can be expressed in microglia is shown, suggesting roles for telomersase in micro glial responses to brain injury.
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Homocysteine and folate deficiency sensitize oligodendrocytes to the cell death-promoting effects of a presenilin-1 mutation and amyloid β-peptide

TL;DR: Roles for homocysteine and folate deficiency in the white matter damage in AD and related neurodegenerative disorders are suggested.
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Knockdown of FABP5 mRNA decreases cellular cholesterol levels and results in decreased apoB100 secretion and triglyceride accumulation in ARPE-19 cells

TL;DR: The results indicate that FABP5 mRNA knockdown results in the accumulation of cellular triglycerides, decreased cholesterol levels, and reduced secretion of apoB100 protein and lipoprotein-like particles, suggesting that F ABP5 plays a critical role in lipid metabolism in RPE cells, suggesting the downregulation in the RPE/choroid complex in vivo might contribute to aging and early age-related macular degeneration.