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Research

30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 76–99 of 99 studies in TREM2 and immune genetics published 2020 (page 4 of 4) · 30,180 in the whole library · How the 0–100 score works

Download bibliography of these 99 studies, in this order: BibTeX (.bib) · RIS (.ris)

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; 15,654 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.

A reporter cell system for the triggering receptor expressed on myeloid cells 2 reveals differential effects of disease-associated variants on receptor signaling and activation by antibodies against the stalk region

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Glia 2020-12-14

The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor expressed on myeloid-derived cell types. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Peripherally derived angiotensin converting enzyme-enhanced macrophages alleviate Alzheimer-related disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Brain : a journal of neurology 2020-01-01

The combined in vivo approaches showed that increased cerebral infiltration of ACE10 as compared to wild-type monocytes (∼3-fold increase; P < 0.05) led to reductions in cerebral soluble amyloid-β1-42, vascular and parenchymal amyloid-β deposits, and astrocytosis (31%, 47-80%, and 33%, respectively; P < 0.05-0.0001). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Diabetic phenotype in mouse and humans reduces the number of microglia around β-amyloid plaques

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Molecular neurodegeneration 2020-11-10

To evaluate whether the mouse model-derived results translate to human patients, the effects of diabetic phenotype on microglial pathology were assessed in cortical biopsies of idiopathic normal pressure hydrocephalus (iNPH) patients encompassing β-amyloid pathology. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Examination of the Effect of Rare Variants in TREM2, ABI3, and PLCG2 in LOAD Through Multiple Phenotypes

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer's disease : JAD 2020-01-01

The results of this study highlight the importance of including biomarkers and alternative phenotypes to better understand the role of novel candidate genes with the disease. 5 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

Shifting paradigms: The central role of microglia in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurobiology of disease 2020-06-12

Recent human genetic studies have challenged long standing hypotheses about the chain of events in Alzheimer's disease (AD), as the identification of genetic risk factors in microglial genes supports a causative role for microglia in the disease. 4 key findings →

Evidence: low

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

Triggering receptor expressed on myeloid cells 2 activation downregulates toll-like receptor 4 expression and ameliorates cognitive impairment in the Aβ1-42 -induced Alzheimer's disease mouse model

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Synapse (New York, N.Y.) 2020-06-12

Increasing evidence suggests that changes in the triggering receptor expressed on myeloid cells 2 (TREM2) is closely correlated with the pathological development of Alzheimer's disease (AD). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Peripheral TREM2 mRNA levels in early and late-onset Alzheimer disease's patients

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Molecular biology reports 2020-07-17

'Triggering receptor expressed on myeloid cells 2' (TREM2) gene is involved in Alzheimer's disease (AD) and TREM2 mRNA expression is known to be increased in the peripheral blood cells of AD patients. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Meprin β cleaves TREM2 and controls its phagocytic activity on macrophages

✓ Peer-reviewed alzhub usefulness score 39 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2020-04-01

The triggering receptor expressed on myeloid cells 2 (TREM2) is a multifunctional surface protein that affects survival, migration, and phagocytic capacity of myeloid cells. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Potential Therapeutic Approaches for Cerebral Amyloid Angiopathy and Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 39 out of 100. International journal of molecular sciences 2020-03-14

Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease directly implicated in Alzheimer's disease (AD) pathogenesis through amyloid-β (Aβ) deposition, which may cause the development and progression of dementia. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Activation of FAK/Rac1/Cdc42-GTPase signaling ameliorates impaired microglial migration response to Aβ42 in triggering receptor expressed on myeloid cells 2 loss-of-function murine models

✓ Peer-reviewed alzhub usefulness score 38 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2020-07-01

Mutation of Triggering receptor expressed on myeloid cells 2 (TREM2) impairs the response of microglia to amyloid-β (Aβ) pathology in Alzheimer's disease (AD), although the mechanism governing TREM2-regulated microglia recruitment to Aβ plaques remains unresolved. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Bilberry anthocyanins improve neuroinflammation and cognitive dysfunction in APP/PSEN1 mice via the CD33/TREM2/TYROBP signaling pathway in microglia

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Food & function 2020-02-01

Alzheimer's disease, characterized by neuroinflammation and beta-amyloid protein plaques, is a memory-threatening neurodegenerative disease with no effective treatment. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Geniposide Enhances Macrophage Autophagy through Downregulation of TREM2 in Atherosclerosis

✓ Peer-reviewed alzhub usefulness score 38 out of 100. The American journal of Chinese medicine 2020-12-10

Macrophage autophagy defect is closely related to the progression of atherosclerosis (AS) and is regulated by the triggering receptor expressed on myeloid cell 2 (TREM2). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Weighted burden analysis of exome-sequenced late-onset Alzheimer's cases and controls provides further evidence for a role for PSEN1 and suggests involvement of the PI3K/Akt/GSK-3β and WNT signalling pathways

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Annals of human genetics 2020-02-05

Previous studies have implicated common and rare genetic variants as risk factors for late-onset Alzheimer's disease (LOAD). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.

1,037 records (3.4% of the library) are not peer-reviewed — 964 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