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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 37 studies in TREM2 and immune genetics with an author at University College London (GB) (page 1 of 2) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Other subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Other institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

What “TREM2 and immune genetics” covers

TREM2 and immune genetics — The TREM2 gene and related immune pathways in the brain, and what they mean for risk and treatment.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

TREM2 variants in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 85 out of 100. The New England journal of medicine 2012-11-14

Homozygous loss-of-function mutations in TREM2, encoding the triggering receptor expressed on myeloid cells 2 protein, have previously been associated with an autosomal recessive form of early-onset dementia. 4 key findings →

Design: meta-analysis Participants: 1,092 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Plasma GFAP is an early marker of amyloid-β but not tau pathology in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 78 out of 100. Brain : a journal of neurology 2021-12-01

Although recent clinical trials targeting amyloid-β in Alzheimer's disease have shown promising results, there is increasing evidence suggesting that understanding alternative disease pathways that interact with amyloid-β metabolism and amyloid pathology might be important to halt the clinical deterioration. 4 key findings →

Design: longitudinal study Participants: 75 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Microglial activation and tau propagate jointly across Braak stages

✓ Peer-reviewed alzhub usefulness score 77 out of 100. Nature medicine 2021-08-26

Compelling experimental evidence suggests that microglial activation is involved in the spread of tau tangles over the neocortex in Alzheimer's disease (AD). 4 key findings →

Design: longitudinal study Participants: 130 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

sTREM2 cerebrospinal fluid levels are a potential biomarker for microglia activity in early-stage Alzheimer's disease and associate with neuronal injury markers

✓ Peer-reviewed alzhub usefulness score 60 out of 100. EMBO molecular medicine 2016-05-02

TREM2 is an innate immune receptor expressed on the surface of microglia. 4 key findings →

Design: cross-sectional Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Increased cerebrospinal fluid soluble TREM2 concentration in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Molecular neurodegeneration 2016-01-12

The discovery that heterozygous missense mutations in the gene encoding triggering receptor expressed on myeloid cells 2 (TREM2) are risk factors for Alzheimer's disease (AD), with only the apolipoprotein E (APOE) ε4 gene allele conferring a higher risk, has led to increased interest in immune biology in the brain. 4 key findings →

Participants: 37 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Microglial activation protects against accumulation of tau aggregates in nondemented individuals with underlying Alzheimer's disease pathology

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Nature aging 2022-11-28

The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD) 1 . 4 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Xenografted human microglia display diverse transcriptomic states in response to Alzheimer's disease-related amyloid-β pathology

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Nature neuroscience 2024-03-27

Microglia are central players in Alzheimer's disease pathology but analyzing microglial states in human brain samples is challenging due to genetic diversity, postmortem delay and admixture of pathologies. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Single-cell RNA sequencing-derived signatures define response patterns to atezolizumab + bevacizumab in advanced hepatocellular carcinoma

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Journal of hepatology 2024-12-19

& aims The combination of atezolizumab and bevacizumab (atezo+bev) is the current standard of care for advanced hepatocellular carcinoma (HCC), providing a median overall survival (OS) of 19.2 months. 4 key findings →

Participants: 317 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Cerebrospinal fluid soluble TREM2 levels in frontotemporal dementia differ by genetic and pathological subgroup

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Alzheimer's research & therapy 2018-08-16

Reliable biomarkers of frontotemporal dementia (FTD) are currently lacking. 4 key findings →

Design: longitudinal study Participants: 20 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

R47H TREM2 variant increases risk of typical early-onset Alzheimer's disease but not of prion or frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2014-08-23

We confirm only p.R47H as a risk factor for AD (odds ratio or OR = 2.19; 95% confidence interval or CI = 1.04-4.51; P = .03). p.R47H does not significantly alter risk for frontotemporal dementia (OR = 0.81), variant or sporadic CJD (OR = 1.06 95%CI = 0.66-1.69) in our cohorts. 4 key findings →

Participants: 700 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Trem2 expression in microglia is required to maintain normal neuronal bioenergetics during development

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Immunity 2023-12-29

Triggering receptor expressed on myeloid cells 2 (Trem2) is a myeloid cell-specific gene expressed in brain microglia, with variants that are associated with neurodegenerative diseases, including Alzheimer's disease. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

The role of TREM2 in Alzheimer's disease and other neurodegenerative disorders

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The Lancet. Neurology 2018-07-17

Alzheimer's disease is a genetically complex disorder; rare variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene have been shown to as much as triple an individual's risk of developing Alzheimer's disease. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

AD-linked R47H-TREM2 mutation induces disease-enhancing microglial states via AKT hyperactivation

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Science translational medicine 2021-12-01

The hemizygous R47H variant of triggering receptor expressed on myeloid cells 2 ( TREM2 ), a microglia-specific gene in the brain, increases risk for late-onset Alzheimer’s disease (AD). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Trem2 promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Human molecular genetics 2020-11-01

Genome-wide association studies have reported that, amongst other microglial genes, variants in TREM2 can profoundly increase the incidence of developing Alzheimer's disease (AD). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

CSF concentrations of soluble TREM2 as a marker of microglial activation in HIV-1 infection

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurology(R) neuroimmunology & neuroinflammation 2018-11-07

CSF sTREM2 increased with systemic and CNS HIV-1 disease severity, with the highest levels found in patients with HIV-associated dementia (HAD). 4 key findings →

Design: cross-sectional Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Novel compound heterozygous mutation in TREM2 found in a Turkish frontotemporal dementia-like family

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurobiology of aging 2013-07-17

Triggering receptor expressed on myeloid cells 2 (TREM2) homozygous mutations cause Nasu-Hakola disease, an early-onset recessive form of dementia preceded by bone cysts and fractures. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

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Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed