- 701studies on this subject, of 27,380 in the library
- 684peer-reviewed
- 2001–2026years published
- 47median usefulness score out of 100
These counts and lists are worked out from the library itself each time the page loads. A score rates how much weight a study can bear — its design, journal, evidence and recency — not whether its result is good news. How we score a study. For a plain-English guide to this subject, see Genetics.
The 20 highest-scoring studies
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TREM2 variants in Alzheimer's disease
This genetic study sequenced the TREM2 gene in 1,092 people with Alzheimer's disease and 1,107 controls. It pooled data on one TREM2 variant, R47H, from three genome-wide studies and checked that variant in a further 1,887 cases and 4,061 controls. The summary held here describes the methods but not the results, so see the original paper for what was found. It is a genetics study and does not test any treatment, cure, or prevention.
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Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease
In a three-stage genetic study of 85,133 people, the authors found three new protein-changing variants linked to Alzheimer's disease, including "a protective variant in PLCG2" (odds ratio 0.68, rarer in people with Alzheimer's than in controls) and "a risk variant in ABI3". The authors say the findings "implicate microglial-mediated innate immunity", meaning the brain's immune cells. These are rare-variant associations, not causes, and the study tests no treatment or prevention.
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Plasma GFAP is an early marker of amyloid-β but not tau pathology in Alzheimer's disease
This longitudinal study found that plasma GFAP was an early marker of amyloid-beta but not tau pathology in Alzheimer's disease. It concerns a biomarker and does not test a treatment, cure or prevention.
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Microglial activation and tau propagate jointly across Braak stages
In 130 living people, microglial activation and tau accumulation were found to spread together across the brain in a Braak-like pattern. This links microglial activation to tau spread but does not test any treatment.
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Multi-ancestry genome-wide meta-analysis of 56,241 individuals identifies known and novel cross-population and ancestry-specific associations as novel risk loci for Alzheimer's disease
Pooling genetic data from 56,241 people of White, African American, Hispanic and East Asian ancestry, this study found 13 gene regions linked to late-onset Alzheimer's across populations, including two new ones near LRRC4C and LHX5-AS1, plus population-specific regions near PTPRK, GRB14 and KIAA0825. The authors say including diverse ancestries boosts the power to find risk genes, which can point to new biological pathways to study.
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The role of TREM2 R47H as a risk factor for Alzheimer's disease, frontotemporal lobar degeneration, amyotrophic lateral sclerosis, and Parkinson's disease
This study tested a rare change in the TREM2 gene, called R47H, in 19,940 new people of European descent and pooled them with 28 earlier data sets. Across 24,086 people with Alzheimer's disease and 148,993 without, carriers had about 2.7 times the odds of having Alzheimer's (odds ratio 2.71). The study also looked at three other brain diseases and at amyloid and tau in spinal fluid, but those results are not in our record; it shows a genetic association in European-descent samples, not a cause, and reports no treatment or prevention.
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Variant of TREM2 associated with the risk of Alzheimer's disease
This genetic study sequenced the genomes of 2,261 Icelanders to look for rare variants likely to affect protein function. It then tested those variants in people with and without Alzheimer's disease, and checked them in case-control groups from the United States, Norway, the Netherlands and Germany. The authors report a TREM2 variant associated with Alzheimer's disease risk, but the summary held here stops before the results, so see the original paper for which variant and how large the effect is. It identifies a genetic risk association and does not test any treatment, cure, or prevention.
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Assessing the role of the TREM2 p.R47H variant as a risk factor for Alzheimer's disease and frontotemporal dementia
This multi-center study found that the TREM2 p.R47H variant was more common in Alzheimer's disease patients than controls, confirming it as a risk factor. It is a genetic association study and does not test any treatment or prevention.
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A Path Toward Precision Medicine for Neuroinflammatory Mechanisms in Alzheimer's Disease
This review brings together earlier gene and protein studies on brain inflammation in Alzheimer's disease. It lists genes found in large genetic studies (TREM2, CD33, CR1, CLU, ABCA7 and others) that are "potentially linked" to inflammation, and it names microglia and astrocytes as "key cellular drivers and regulators" of that process. It is a map for future research toward tailored treatment: it reports no new data, no patients and no treatment result, and it does not show that these genes cause the disease.
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Loss of TREM2 function increases amyloid seeding but reduces plaque-associated ApoE
In mice, losing TREM2 function increased the early seeding of amyloid plaques and reduced microglial clustering and ApoE around new plaques. This suggests TREM2 and microglia affect how amyloid plaques begin to form, but it is animal and human tissue work, not a treatment.
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Preclinical and first-in-human evaluation of AL002, a novel TREM2 agonistic antibody for Alzheimer's disease
This paper reports preclinical and first-in-human evaluation of AL002, an antibody designed to activate TREM2, which is thought to enhance clearance of amyloid beta. It is an early-stage clinical trial, so it does not yet show that the treatment alters the course of Alzheimer's disease.
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Meta-Analysis of Leukocyte Diversity in Atherosclerotic Mouse Aortas
This meta-analysis of mouse aorta studies confirms a Trem2 foamy macrophage subset among leukocytes in atherosclerosis. It concerns heart vessel disease, not Alzheimer's, and offers no Alzheimer's treatment insight.
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TREM2 R47H variant and risk for Alzheimer's disease: assessment in a Greek population and updated meta-analysis
In a Greek sample of 327 people with Alzheimer's and 700 healthy controls, the TREM2 R47H variant was found in three patients and no controls, a significant association. An updated meta-analysis of 27 studies linked the variant to Alzheimer's with an odds ratio of 2.98, with a similar odds ratio of 2.93 in Caucasian-only studies, while Asian studies showed no significant link. This supports R47H as a genetic risk factor in Caucasian populations.
- Neuroimaging biomarkers and CSF sTREM2 levels in Alzheimer's disease: a longitudinal study
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Early increase of CSF sTREM2 in Alzheimer's disease is associated with tau related-neurodegeneration but not with amyloid-β pathology
Soluble TREM2 in spinal fluid is a stand-in measure of how microglia, the brain's immune cells, are working. This cross-sectional study grouped people at early stages of Alzheimer's, with and without symptoms, using the NIA-AA biomarker framework. It reports that sTREM2 is raised early and that the rise is associated with tau-related neurodegeneration but not with amyloid-β pathology. The stored text gives no figures, and as a one-time observational comparison it shows association rather than cause and tests no treatment.
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Missense variant in TREML2 protects against Alzheimer's disease
This meta-analysis examined a missense variant in TREML2 and reported that it protects against Alzheimer's disease. It identifies a genetic factor linked to disease risk but does not test any treatment or prevention in people.
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A candidate regulatory variant at the TREM gene cluster associates with decreased Alzheimer's disease risk and increased TREML1 and TREM2 brain gene expression
This study found that a variant near TREM2, rs9357347-C, was associated with reduced Alzheimer's disease risk and increased TREML1 and TREM2 brain gene expression. It identifies a possible genetic link but does not provide a treatment or cure.
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Resveratrol Attenuates CSF Markers of Neurodegeneration and Neuroinflammation in Individuals with Alzheimer's Disease
This sub-analysis of a phase 2 trial looked at spinal fluid from 30 people with Alzheimer's given resveratrol and 21 given placebo over 52 weeks. Resveratrol was linked to lower levels of markers of nerve damage and inflammation, including TREM2 and MMP-9. The authors say resveratrol may have anti-inflammatory and protective effects, but whether these biomarker changes translate into clinical benefit still needs study.
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TREM2 is associated with increased risk for Alzheimer's disease in African Americans
Earlier studies linked rare TREM2 gene variants to late-onset Alzheimer's disease in people of European origin; this study tested six such variants in African Americans (906 people with Alzheimer's and 2,487 without). One variant, p.L211P, was modestly more common in people with Alzheimer's (odds ratio 1.27, 95% CI 1.05–1.54), while p.W191X showed only a non-significant trend (odds ratio 1.35, 95% CI 0.97–1.87). This is a genetic association in one population, not a cause, and it reports no treatment, cure or prevention.
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PLCG2 protective variant p.P522R modulates tau pathology and disease progression in patients with mild cognitive impairment
In 3595 patients with mild cognitive impairment, carriers of the PLCG2 p.P522R variant showed a slower rate of cognitive decline than non-carriers. This is an observational genetic study and reports no treatment, cure or prevention.
See all 701 studies in TREM2 and immune genetics, with filters →
Newest additions on this subject
- Soluble TREM2 suppresses neuronal activity
- NADPH attenuates tau pathology and disease-associated microglial phenotype in a truncated tau- induced mouse model
- Electroacupuncture alleviate cognitive impairment via activation of TREM2-positive microglia in APP/PS1 mice
- DAP12-deficient microglia adopt a TREM2-independent antigen-presenting state with a glial-to-neuronal cascade in Nasu-Hakola disease
- MTHFR*677C>T produces distinct prodromal disease signatures in a mouse model of late-onset Alzheimer’s disease
- Cross-Dataset Reanalysis of Mouse Alzheimer Disease Single-Cell RNA-Sequencing Data Reveals a Reproducible Innate Immune Activation Signature
- Context-dependent TREM2 signalling in myeloid cells: Molecular mechanisms and immunotherapeutic divergence in neurodegeneration and cancer
- A self-limiting, TREM2-dependent anabolic program confers microglial resilience in Alzheimer’s disease
- A sphingomyelin-cholesterol complex regulates TLR4 activation in microglia
- Public-Data Reanalysis Links MS4A4A to M2-like Human Myeloid States and Supports a Predicted Four-Pass Transmembrane Fold
All 701 studies in TREM2 and immune genetics, newest first →
What the library holds on this subject
By review status
| Status | Studies |
|---|---|
| Peer-reviewed | 684 |
| Preprint — not yet peer-reviewed | 17 |
By strength of evidence
| Rated in our summary | Studies |
|---|---|
| low | 612 |
| moderate | 51 |
| high | 31 |
| not rated | 7 |
Most frequent journals
| Journal | Studies |
|---|---|
| Molecular neurodegeneration | 37 |
| Neurobiology of aging | 27 |
| Journal of neuroinflammation | 22 |
| Alzheimer's & dementia : the journal of the Alzheimer's Association | 21 |
| Neuron | 16 |
| The Journal of experimental medicine | 15 |
| Acta neuropathologica | 13 |
| Molecular neurobiology | 13 |
| Nature communications | 13 |
| Frontiers in aging neuroscience | 12 |
Studies by year published
| Year | Studies | Bar |
|---|---|---|
| 2026 | 20 | |
| 2025 | 31 | |
| 2024 | 48 | |
| 2023 | 59 | |
| 2022 | 70 | |
| 2021 | 73 | |
| 2020 | 78 | |
| 2019 | 58 | |
| 2018 | 60 | |
| 2017 | 46 | |
| 2016 | 42 | |
| 2015 | 30 | |
| 2014 | 21 | |
| 2013 | 21 | |
| 2012 | 6 | |
| 2011 | 1 | |
| 2010 | 7 | |
| 2009 | 4 | |
| 2008 | 7 | |
| 2007 | 3 | |
| 2006 | 2 | |
| 2005 | 4 | |
| 2004 | 2 | |
| 2003 | 5 | |
| 2002 | 2 | |
| 2001 | 1 |
Counts the 701 studies with a usable publication date. The library is a large sample of published work, not a complete index, so these counts describe the library, not the whole field.
Other subjects in the library
- Getting a diagnosis
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- Clinical safety
- Health systems and care delivery
- End-of-life care
- Risk factors
- Digital health tools
- Treatments
- Disparities
- Mild cognitive impairment
- Risk genes beyond APOE
- Brain scans and imaging
- Cognitive tests and assessment
- Lewy body dementia
- Down syndrome and Alzheimer's
- Long-term cohort studies
- Inflammation and the immune system
- Tau biomarkers
- Brain tissue and pathology
- Drug development
- Hippocampus size on brain scans