Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

TREM2: Keeping Microglia Fit during Good Times and Bad.

Cell metabolism - 3 Oct 2017

Hong Soyon, Stevens Beth

Abstract excerpt

Microglia are the macrophages of the brain and play an important role in Alzheimer's disease (AD). In Cell, Ulland et al. (2017) recently reported that mutations in TREM2, a protein implicated in AD, disrupt microglial energy state and function, thus sabotaging the microglia's ability to defend the brain against amyloid plaques.

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer Disease
Share to Gene Deletion
Share to Gene Expression Regulation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Membrane Glycoproteins

Share to Microglia

Share to Plaque, Amyloid

Share to Receptors, Immunologic

Share to TOR Serine-Threonine Kinases

Source

Identifiers

PMID: 28978423
DOI: 10.1016/j.cmet.2017.09.010

Genes

TREM2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TREM2: Keeping Microglia Fit during Good Times and Bad.PMID 28978423Read ↗

TREM2 lipid sensing sustains the microglial response in an Alzheimer's disease model.Semantic proximity Read ↗

TREM2 variants: new keys to decipher Alzheimer disease pathogenesis.Semantic proximity Read ↗

A locked immunometabolic switch underlies TREM2 R47H loss of function in human iPSC--derived microgliaSemantic proximity Read ↗

TREM2 expression level is critical for microglial state, metabolic capacity and efficacy of TREM2 agonismSemantic proximity Read ↗

Homeostatic microglia initially seed and activated microglia later reshape amyloid plaques in Alzheimer's Disease.Semantic proximity Read ↗

The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases.Semantic proximity Read ↗

Role of TREM2 in Alzheimer's Disease: A Long Road Ahead.Semantic proximity Read ↗

Microglia Gravitate toward Amyloid Plaques Surrounded by Externalized Phosphatidylserine via TREM2Semantic proximity Read ↗

The dual role of microglia in Alzheimer’s disease: from immune regulation to pathological progressionSemantic proximity Read ↗

Humanized TREM2 mice reveal microglia-intrinsic and -extrinsic effects of R47H polymorphism.Semantic proximity Read ↗

Phagocytes as Plaque Catalysts: Human Macrophages Actively Generate Pathogenic Aβ42 Fibrils with Seeding and Cross-Seeding PotencySemantic proximity Read ↗

CSF Soluble TREM2 Concentrations Correlate With the Severity of Neurofibrillary Degeneration, Cognitive Impairment, and Inflammasome Activation in Alzheimer’s DiseaseSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.