ReviewOxidative medicine and cellular longevity2013
The triggering receptor expressed on myeloid cells 2: "TREM-ming" the inflammatory component associated with Alzheimer's disease.
Review in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Targeting TREM2 for Parkinson's Disease: Where to Go?Frontiers in immunology · 2021Pooled it
- Shared and disease-specific pathways in frontotemporal dementia and Alzheimer's and Parkinson's diseases.Nature medicine · 2025Article
- Navigating the treatment landscape of Alzheimer's disease: Current strategies and future directions.Ibrain · 2025Review
- Article
- Alzheimer's disease risk after COVID-19: a view from the perspective of the infectious hypothesis of neurodegeneration.Neural regeneration research · 2023Review
- Mapping Molecular Networks withinPharmaceuticals (Basel, Switzerland) · 2022Article
- Hydroxysafflor Yellow A Inhibits AβNeurochemical research · 2022Article
- Plaque-associated human microglia accumulate lipid droplets in a chimeric model of Alzheimer's disease.Molecular neurodegeneration · 2021Article
- The most prevalent rare coding variants of TREM2 conferring risk of Alzheimer's disease: A systematic review and meta-analysis.Experimental and therapeutic medicine · 2021Article
- Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?Nature reviews. Neurology · 2021Review
- Ferroptosis Mediated by Lipid Reactive Oxygen Species: A Possible Causal Link of Neuroinflammation to Neurological Disorders.Oxidative medicine and cellular longevity · 2021Review
- Investigation of pathology, expression and proteomic profiles in human TREM2 variant postmortem brains with and without Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2020Article
- TREM2 Attenuates Aβ1-42-Mediated Neuroinflammation in BV-2 Cells by Downregulating TLR Signaling.Neurochemical research · 2019Article
- Heterozygous carriers of galactocerebrosidase mutations that cause Krabbe disease have impaired microglial function and defective repair of myelin damage.Neural regeneration research · 2018Review
- Heterozygote galactocerebrosidase (GALC) mutants have reduced remyelination and impaired myelin debris clearance following demyelinating injury.Human molecular genetics · 2017Article
- Overview and Current Status of Alzheimer's Disease in Bangladesh.Journal of Alzheimer's disease reports · 2017Review
- Alzheimer's Disease: From Genetic Variants to the Distinct Pathological Mechanisms.Frontiers in molecular neuroscience · 2017Review
- Neuroimaging Feature Terminology: A Controlled Terminology for the Annotation of Brain Imaging Features.Journal of Alzheimer's disease : JAD · 2017Article
- Alzheimer Disease and Its Growing Epidemic: Risk Factors, Biomarkers, and the Urgent Need for Therapeutics.Neurologic clinics · 2016Review
- TREM2 upregulation correlates with 5-hydroxymethycytosine enrichment in Alzheimer's disease hippocampus.Clinical epigenetics · 2016Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by a progressive loss of memory and cognitive skills. Although much attention has been devoted concerning the contribution of the microscopic lesions, senile plaques, and neurofibrillary tangles to the disease process, inflammation has long been suspected to play a major role in the etiology of AD. Recently, a novel variant in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) has been identified that has refocused the spotlight back onto inflammation as a major contributing factor in AD. Variants in TREM2 triple one's risk of developing late-onset AD. TREM2 is expressed on microglial cells, the resident macrophages in the CNS, and functions to stimulate phagocytosis on one hand and to suppress cytokine production and inflammation on the other hand. The purpose of this paper is to discuss these recent developments including the potential role that TREM2 normally plays and how loss of function may contribute to AD pathogenesis by enhancing oxidative stress and inflammation within the CNS. In this context, an overview of the pathways linking beta-amyloid, neurofibrillary tangles (NFTs), oxidative stress, and inflammation will be discussed.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.