ReviewAlzheimer's research & therapy2013
Alzheimer's disease risk alleles in TREM2 illuminate innate immunity in Alzheimer's disease.
Review in Alzheimer's research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- Multiple Roles of Apolipoprotein E4 in Oxidative Lipid Metabolism and Ferroptosis During the Pathogenesis of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2024Review
- Soluble TREM2 in body fluid in Alzheimer's disease and Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Heparan sulfate proteoglycan in Alzheimer's disease: aberrant expression and functions in molecular pathways related to amyloid-β metabolism.American journal of physiology. Cell physiology · 2023Review
- TREM2 ectodomain and its soluble form in Alzheimer's disease.Journal of neuroinflammation · 2020Review
- High-affinity interactions and signal transduction between Aβ oligomers and TREM2.EMBO molecular medicine · 2018Article
- Glial Draper Rescues Aβ Toxicity in aThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- TREM2-Ligand Interactions in Health and Disease.Journal of molecular biology · 2017Review
- Genomic variants, genes, and pathways of Alzheimer's disease: An overview.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2017Review
- Article
- Targeting innate immunity for neurodegenerative disorders of the central nervous system.Journal of neurochemistry · 2016Review
- The triggering receptor expressed on myeloid cells 2 (TREM2) is associated with enhanced inflammation, neuropathological lesions and increased risk for Alzheimer's dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2015Article
- The Alzheimer disease protective mutation A2T modulates kinetic and thermodynamic properties of amyloid-β (Aβ) aggregation.The Journal of biological chemistry · 2014Article
- The Role of TREM2 in Alzheimer's Disease and Other Neurological Disorders.Journal of Alzheimer's disease & Parkinsonism · 2014Article
- The triggering receptor expressed on myeloid cells (TREM) in inflammatory bowel disease pathogenesis.Journal of translational medicine · 2014Review
- Preparation, crystallization, and preliminary crystallographic analysis of wild-type and mutant human TREM-2 ectodomains linked to neurodegenerative and inflammatory diseases.Protein expression and purification · 2014Article
- Progress in Alzheimer's disease research circa 2013: Is the glass half empty or half full?Alzheimer's research & therapy · 2013Article
- The innate immune system in Alzheimer's disease.International journal of cell biology · 2013Review
- TREM2 signaling, miRNA-34a and the extinction of phagocytosis.Frontiers in cellular neuroscience · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Genetic studies have provided the best evidence for cause and effect relationships in Alzheimer's disease (AD). Indeed, the identification of deterministic mutations in the APP, PSEN1 and PSEN2 genes and subsequent preclinical studies linking these mutations to alterations in Aβ production and aggregation have provided pivotal support for the amyloid cascade hypothesis. In addition, genetic, pathologic and biological studies of APOE have also indicated that the genetic risk for AD associated with APOE4 can be attributed, at least in part, to its pro-amyloidogenic effect on Aβ. In recent years a number of SNPs that show unequivocal genome-wide association with AD risk have implicated novel genetic loci as modifiers of AD risk. However, the functional implications of these genetic associations are largely unknown. For almost all of these associations, the functional variants have not been identified. Very recently, two large consortiums demonstrated that rare variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene confer significant risk for AD. TREM2 is a type 1 membrane receptor protein primarily expressed on microglia in the central nervous system that has been shown to regulate phagocytosis and activation of monocytes. Previously it had been shown that homozygous loss of function mutations in TREM2 cause polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL, Nasu Hakola disease) and also a pure form of early-onset dementia. The association of TREM2 variants with AD brings innate immune signaling into the light, affirming innate immunity's role as a significant factor in AD pathogenesis.
Identifiers
What OpenQuestion holds
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.