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Research

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

Find studies

Showing 1–21 of 21 studies in TREM2 and immune genetics with an author at Icahn School of Medicine at Mount Sinai (US) · 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.

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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.

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

✓ Peer-reviewed alzhub usefulness score 77 out of 100. Genome biology 2025-07-17

Using cross-population GWAS meta-analyses, we identify novel LOAD susceptibility loci in/near LRRC4C and LHX5-AS1, both with known roles in neuronal development, as well as several novel population-unique loci. 1 key finding →

Design: meta-analysis Participants: 409,589 Evidence: high

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

Proteo-genomics of soluble TREM2 in cerebrospinal fluid provides novel insights and identifies novel modulators for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Molecular neurodegeneration 2024-01-03

Triggering receptor expressed on myeloid cells 2 (TREM2) plays a critical role in microglial activation, survival, and apoptosis, as well as in Alzheimer's disease (AD) pathogenesis. 4 key findings →

Participants: 3,350 Evidence: low

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

Assessment of the Genetic Architecture of Alzheimer's Disease Risk in Rate of Memory Decline

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Journal of Alzheimer's disease : JAD 2018-01-01

Many genetic studies for Alzheimer's disease (AD) have been focused on the identification of common genetic variants associated with AD risk and not on other aspects of the disease, such as age at onset or rate of dementia progression. 4 key findings →

Design: longitudinal study Evidence: moderate

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

Prolonged hypernutrition impairs TREM2-dependent efferocytosis to license chronic liver inflammation and NASH development

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Immunity 2022-12-14

Obesity-induced chronic liver inflammation is a hallmark of nonalcoholic steatohepatitis (NASH)-an aggressive form of nonalcoholic fatty liver 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

A novel tau-based rhesus monkey model of Alzheimer's pathogenesis

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2021-03-18

Alzheimer's disease (AD) is a devastating condition with no effective treatments, with promising findings in rodents failing to translate into successful therapies for patients. 4 key findings →

Evidence: low

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

Single-Cell Gene-Regulatory Networks of Advanced Symptomatic Atherosclerosis

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Circulation research 2024-04-19

Single-cell RNA sequencing data generated with SmartSeq2 (≈8000 genes/cell) in 16 588 single cells isolated during atherosclerosis progression in Ldlr -/- Apob 100/100 mice with human-like plasma lipoproteins and from humans with asymptomatic and symptomatic carotid plaques was clustered into multiple subtypes. 4 key findings →

Evidence: low

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

Deficiency of TYROBP, an adapter protein for TREM2 and CR3 receptors, is neuroprotective in a mouse model of early Alzheimer's pathology

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2017-06-13

Conventional genetic approaches and computational strategies have converged on immune-inflammatory pathways as key events in the pathogenesis of late onset sporadic Alzheimer's disease (LOAD). 4 key findings →

Evidence: low

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

Microglial TYROBP/DAP12 in Alzheimer's disease: Transduction of physiological and pathological signals across TREM2

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Molecular neurodegeneration 2022-08-24

TYROBP (also known as DAP12 or KARAP) is a transmembrane adaptor protein initially described as a receptor-activating subunit component of natural killer (NK) cells. 4 key findings →

Evidence: low

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

Phenotypes and ontogeny of senescent hepatic stellate cells in metabolic dysfunction-associated steatohepatitis

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Journal of hepatology 2024-03-18

& aims Hepatic stellate cells (HSCs) are the key drivers of fibrosis in metabolic dysfunction-associated steatohepatitis (MASH), the fastest growing cause of hepatocellular carcinoma (HCC) worldwide. 4 key findings →

Evidence: low

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

Integrative approach to sporadic Alzheimer's disease: deficiency of TYROBP in cerebral Aβ amyloidosis mouse normalizes clinical phenotype and complement subnetwork molecular pathology without reducing Aβ burden

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Molecular psychiatry 2018-10-03

Integrative gene network approaches enable new avenues of exploration that implicate causal genes in sporadic late-onset Alzheimer's disease (LOAD) pathogenesis, thereby offering novel insights for drug-discovery programs. 4 key findings →

Evidence: low

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

Integrative approach to sporadic Alzheimer's disease: deficiency of TYROBP in a tauopathy mouse model reduces C1q and normalizes clinical phenotype while increasing spread and state of phosphorylation of tau

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Molecular psychiatry 2018-10-03

TYROBP/DAP12 forms complexes with ectodomains of immune receptors (TREM2, SIRPβ1, CR3) associated with Alzheimer's disease (AD) and is a network hub and driver in the complement subnetwork identified by multi-scale gene network studies of postmortem human AD brain. 4 key findings →

Evidence: low

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

Reactive or transgenic increase in microglial TYROBP reveals a TREM2-independent TYROBP-APOE link in wild-type and Alzheimer's-related mice

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2020-12-12

Herein, we demonstrate that endogenous Tyrobp transcription is specifically increased in recruited microglia. 4 key findings →

Evidence: low

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

The triggering receptor expressed on myeloid cells 2 (TREM2) is associated with enhanced inflammation, neuropathological lesions and increased risk for Alzheimer's dementia

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2014-12-09

The TREM2 variant is associated with: (i) AD (odds ratio: 4.76; P = .014); (ii) increased density of amyloid plaques and neurofibrillary tangles in multiple brain regions; (iii) increased TREM2 (P = .041) and TYROBP (P = .006) gene expression; (iv) decreased TREM2 protein levels (P = .016); and (v) upregulation of proinflammatory cytokines (regulated on activation, norma 3 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