Over-expressed pathogenic mirnas in Alzheimer's disease (AD) and prion disease (PrD) drive deficits in TREM2-mediated Aβ42 peptide clearance

Frontiers in Aging Neuroscience

Volumn 8, Issue JUN, 2016, Pages

  Zhao, Yuhai ^a,b   Jaber, Vivian ^a   Lukiw, Walter J ^a,b  

^a LOUISIANA STATE UNIVERSITY HEALTH SCIENCES CENTER   (United States)

^b LOUISIANA STATE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

42 amino acid amyloid beta (A 42) peptides; Alzheimer's disease (AD); Creutzfeldt Jakob disease (CJD); Gerstmann Straussler Scheinker syndrome (GSS); Microglial cells; MicroRNA 34a; Phagocytosis; Triggering receptor expressed in myeloid microglial cells (TREM2)

Indexed keywords

AMYLOID BETA PROTEIN[1-42]; MICRORNA 125B; MICRORNA 146A; MICRORNA 155; MICRORNA 34A; MICRORNA 9; TRIGGERING RECEPTOR EXPRESSED ON MYELOID CELLS 2;

ALZHEIMER DISEASE; AMYLOIDOSIS; ANIMAL CELL; ARTICLE; CLEARANCE; CONTROLLED STUDY; CREUTZFELDT JAKOB DISEASE; GERSTMANN STRAUSSLER SCHEINKER SYNDROME; MICROGLIA; MOUSE; NONHUMAN; PHAGOCYTOSIS; PRION DISEASE;

EID: 84980349765     PISSN: None     EISSN: 16634365     Source Type: Journal    
DOI: 10.3389/fnagi.2016.00140     Document Type: Article

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