Reference : TREM2 triggers microglial density and age‐related neuronal loss
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
Systems Biomedicine
TREM2 triggers microglial density and age‐related neuronal loss
Linnartz-Gerlach, Bettina []
Bodea, Liviu-Gabriel []
Klaus, Christine []
Ginolhac, Aurélien mailto [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >]
Halder, Rashi mailto [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > >]
Sinkkonen, Lasse mailto [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >]
Walter, Jochen []
Colonna, Marco []
Neumann, Harald []
John Wiley & Sons
Yes (verified by ORBilu)
[en] The microglial triggering receptor expressed on myeloid cells 2 (TREM2) signals via the activatory membrane adaptor molecule TYROBP. Genetic variants or mutations of TREM2 or TYROBP have been linked to inflammatory neurodegenerative diseases associated with aging. The typical aging process goes along with microglial changes and mild neuronal loss, but the exact contribution of TREM2 is still unclear. Aged TREM2 knock‐out mice showed decreased age‐related neuronal loss in the substantia nigra and the hippocampus. Transcriptomic analysis of the brains of 24 months old TREM2 knock‐out mice revealed 211 differentially expressed genes mostly downregulated and associated with complement activation and oxidative stress response pathways. Consistently, 24 months old TREM2 knock‐out mice showed lower transcription of microglial (Aif1 and Tmem119), oxidative stress markers (Inos, Cyba, and Cybb) and complement components (C1qa, C1qb, C1qc, C3, C4b, Itgam, and Itgb2), decreased microglial numbers and expression of the microglial activation marker Cd68, as well as accumulation of oxidized lipids. Cultured microglia of TREM2 knock‐out mice showed reduced phagocytosis and oxidative burst. Thus, microglial TREM2 contributes to age‐related microglial changes, phagocytic oxidative burst, and loss of neurons with possible detrimental effects during physiological aging.
University of Luxembourg: High Performance Computing - ULHPC
Original publication is available at

File(s) associated to this reference

Fulltext file(s):

Open access
Linnartz-Gerlach_et_al-GLIA2018.pdfPublisher postprint3.54 MBView/Open

Additional material(s):

File Commentary Size Access
Open access
Linnartz-Gerlach_et_al-GLIA2018(SUPPLEMENT).docx792.23 kBView/Open

Bookmark and Share SFX Query

All documents in ORBilu are protected by a user license.