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Research

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

Find studies

Showing 76–100 of 701 studies in TREM2 and immune genetics (page 4 of 29) · 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.

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.

Microglial activation states drive glucose uptake and FDG-PET alterations in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Science translational medicine 2021-10-13

2-Deoxy-2-[ 18 F]fluoro-d-glucose positron emission tomography (FDG-PET) is widely used to study cerebral glucose metabolism. 4 key findings →

Participants: 12 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Heterozygous TREM2 mutations in frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neurobiology of aging 2013-10-16

A causative association was recently demonstrated between homozygous TREM2 mutations and frontotemporal dementia (FTD)-like syndrome and between heterozygous TREM2 exon2 genetic variations and late-onset Alzheimer's disease (AD). 4 key findings →

Participants: 1,030 Evidence: low

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

The effect of increased genetic risk for Alzheimer's disease on hippocampal and amygdala volume

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neurobiology of aging 2016-01-11

Reduction in hippocampal and amygdala volume measured via structural magnetic resonance imaging is an early marker of Alzheimer's disease (AD). 4 key findings →

Design: case-control study Evidence: moderate

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

Increased DNA methylation near TREM2 is consistently seen in the superior temporal gyrus in Alzheimer's disease brain

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neurobiology of aging 2016-07-16

Although mutations within the TREM2 gene have been robustly associated with Alzheimer's disease, it is not known whether alterations in the regulation of this gene are also involved in pathogenesis. 3 key findings →

Design: meta-analysis Evidence: high

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

Differentially expressed genes in Alzheimer's disease highlighting the roles of microglia genes including OLR1 and astrocyte gene CDK2AP1

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Brain, behavior, & immunity - health 2021-02-24

Alzheimer's disease (AD) is associated with abnormal tau and amyloid-β accumulation in the brain, leading to neurofibrillary tangles, neuropil threads and extracellular amyloid-β plaques. 4 key findings →

Design: meta-analysis Evidence: high

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

sTREM2 is associated with amyloid-related p-tau increases and glucose hypermetabolism in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. EMBO molecular medicine 2023-01-09

Microglial activation occurs early in Alzheimer's disease (AD) and previous studies reported both detrimental and protective effects of microglia on AD progression. 4 key findings →

Design: cross-sectional Participants: 70 Evidence: moderate

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

TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2017-10-09

Variants in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) were recently found to increase the risk for developing Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Gene expression and functional deficits underlie TREM2-knockout microglia responses in human models of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Nature communications 2020-10-23

The discovery of TREM2 as a myeloid-specific Alzheimer's disease (AD) risk gene has accelerated research into the role of microglia in AD. 4 key findings →

Evidence: low

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

Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Acta neuropathologica 2019-04-20

Alzheimer's disease (AD) is a progressive neurodegenerative disease in which the formation of extracellular aggregates of amyloid beta (Aβ) peptide, fibrillary tangles of intraneuronal tau and microglial activation are major pathological hallmarks. 4 key findings →

Evidence: low

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

Early-Onset Alzheimer Disease and Candidate Risk Genes Involved in Endolysosomal Transport

✓ Peer-reviewed alzhub usefulness score 56 out of 100. JAMA neurology 2017-09-01

Mutations in APP, PSEN1, and PSEN2 lead to early-onset Alzheimer disease (EOAD) but account for only approximately 11% of EOAD overall, leaving most of the genetic risk for the most severe form of Alzheimer disease unexplained. 4 key findings →

Design: case-control study Evidence: moderate

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

Clearance of apoptotic neurons without inflammation by microglial triggering receptor expressed on myeloid cells-2

✓ Peer-reviewed alzhub usefulness score 55 out of 100. The Journal of experimental medicine 2005-02-01

Elimination of apoptotic neurons without inflammation is crucial for brain tissue homeostasis, but the molecular mechanism has not been firmly established. 4 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