ArticlePloS one2014
Evidence of trem2 variant associated with triple risk of Alzheimer's disease.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Lack of genetic association between TREM2 and Alzheimer's disease in East Asian population: a systematic review and meta-analysis.American journal of Alzheimer's disease and other dementias · 2015Pooled it
- Uncovering the biological mechanisms of TREM2 with molecular simulations: A comprehensive review and perspective.Progress in biophysics and molecular biology · 2026Review
- Omics-driven strategies for identifying biomarkers in Alzheimer's disease.Metabolic brain disease · 2026Review
- The flexible stalk domain of sTREM2 modulates its interactions with brain-based phospholipids.eLife · 2025Article
- Microglial Modulation in Alzheimer's Disease: Central Players in Neuroinflammation and Pathogenesis.Current Alzheimer research · 2025Review
- Ouabain Ameliorates Alzheimer's Disease-Associated Neuropathology and Cognitive Impairment in FADNutrients · 2024Article
- Analysis of nonsynonymous SNPs in candidate genes that influence bovine temperament and evaluation of their effect in Brahman cattle.Molecular biology reports · 2024Article
- Study on pyroptosis-related genes Casp8, Gsdmd and Trem2 in mice with cerebral infarction.PeerJ · 2024Article
- The gut microbiome and Alzheimer's disease: Complex and bidirectional interactions.Neuroscience and biobehavioral reviews · 2022Review
- Microglia in Alzheimer's Disease: An Unprecedented Opportunity as Prospective Drug Target.Molecular neurobiology · 2022Review
- Deciphering the Link Between ERFrontiers in aging neuroscience · 2022Review
- Advances in PPARs Molecular Dynamics and Glitazones as a Repurposing Therapeutic Strategy through Mitochondrial Redox Dynamics against Neurodegeneration.Current neuropharmacology · 2022Review
- TREM2 alters the phagocytic, apoptotic and inflammatory response to AβMolecular immunology · 2021Article
- A MAC2-positive progenitor-like microglial population is resistant to CSF1R inhibition in adult mouse brain.eLife · 2020Article
- Investigation of pathology, expression and proteomic profiles in human TREM2 variant postmortem brains with and without Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2020Article
- Mechanistic insights into the deleterious roles of Nasu-Hakola disease associated TREM2 variants.Scientific reports · 2020Article
- Divergent roles of astrocytic versus neuronal EAAT2 deficiency on cognition and overlap with aging and Alzheimer's molecular signatures.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Opposite microglial activation stages upon loss of PGRN or TREM2 result in reduced cerebral glucose metabolism.EMBO molecular medicine · 2019Article
- Article
- Drug Development for Alzheimer's Disease: Microglia Induced Neuroinflammation as a Target?International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease is one of the main causes of dementia among elderly individuals and leads to the neurodegeneration of different areas of the brain, resulting in memory impairments and loss of cognitive functions. Recently, a rare variant that is associated with 3-fold higher risk of Alzheimer's disease onset has been found. The rare variant discovered is a missense mutation in the loop region of exon 2 of Trem2 (rs75932628-T, Arg47His). The aim of this study was to investigate the evidence for potential structural and functional significance of Trem2 gene variant (Arg47His) through molecular dynamics simulations. Our results showed the alteration caused due to the variant in TREM2 protein has significant effect on the ligand binding affinity as well as structural configuration. Based on molecular dynamics (MD) simulation under salvation, the results confirmed that native form of the variant (Arg47His) might be responsible for improved compactness, hence thereby improved protein folding. Protein simulation was carried out at different temperatures. At 300K, the deviation of the theoretical model of TREM2 protein increased from 2.0 Å at 10 ns. In contrast, the deviation of the Arg47His mutation was maintained at 1.2 Å until the end of the simulation (t = 10 ns), which indicated that Arg47His had reached its folded state. The mutant residue was a highly conserved region and was similar to "immunoglobulin V-set" and "immunoglobulin-like folds". Taken together, the result from this study provides a biophysical insight on how the studied variant could contribute to the genetic susceptibility to Alzheimer's disease.
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