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Research

28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–50 of 78 studies in TREM2 and immune genetics published 2020 (page 2 of 4) · 28,580 in the whole library · How the 0–100 score works

Download bibliography of these 78 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; 14,058 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 activation attenuates neuroinflammation and neuronal apoptosis via PI3K/Akt pathway after intracerebral hemorrhage in mice

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Journal of neuroinflammation 2020-05-28

Neuroinflammation is an important host defense response to secondary brain injury after intracerebral hemorrhage (ICH). 4 key findings →

Participants: 216 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

Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of neuroinflammation 2020-08-14

Triggering receptor expressed on myeloid cell-2 (TREM2) is a lipid and lipoprotein binding receptor expressed by cells of myeloid origin. 4 key findings →

Evidence: high

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

Trem2 Deletion Reduces Late-Stage Amyloid Plaque Accumulation, Elevates the Aβ42:Aβ40 Ratio, and Exacerbates Axonal Dystrophy and Dendritic Spine Loss in the PS2APP Alzheimer's Mouse Model

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2020-01-24

TREM2 is an Alzheimer's disease (AD) risk gene expressed in microglia. 4 key findings →

Evidence: low

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

Dynamic changes of CSF sTREM2 in preclinical Alzheimer's disease: the CABLE study

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Molecular neurodegeneration 2020-04-10

Loss of function of triggering receptor expressed on myeloid cell 2 (TREM2), a key receptor selectively expressed by microglia in the brain, contributes to the development of Alzheimer's disease (AD). 4 key findings →

Evidence: moderate

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

Multi-omic comparison of Alzheimer's variants in human ESC-derived microglia reveals convergence at APOE

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of experimental medicine 2020-12-01

Variations in many genes linked to sporadic Alzheimer's disease (AD) show abundant expression in microglia, but relationships among these genes remain largely elusive. 4 key findings →

Evidence: low

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

Alzheimer's-associated PLCγ2 is a signaling node required for both TREM2 function and the inflammatory response in human microglia

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nature neuroscience 2020-06-08

Human genetic data indicate that microglial dysfunction contributes to the pathology of Alzheimer's disease (AD), exemplified by the identification of coding variants in triggering receptor expressed on myeloid cells 2 (TREM2) and, more recently, in PLCG2, a phospholipase-encoding gene expressed in microglia. 4 key findings →

Evidence: low

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

The substrate repertoire of γ-secretase/presenilin

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Seminars in cell & developmental biology 2020-06-29

The intramembrane protease γ-secretase is a hetero-tetrameric protein complex with presenilin as the catalytic subunit and cleaves its membrane protein substrates within their single transmembrane domains. γ-Secretase is well known for its role in Notch signalling and in Alzheimer's disease, where it catalyzes the formation of the pathogenic amyloid β (Aβ) peptide. 4 key findings →

Evidence: low

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

TREM2 ameliorates neuroinflammatory response and cognitive impairment via PI3K/AKT/FoxO3a signaling pathway in Alzheimer's disease mice

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Aging 2020-10-16

Triggering receptor expressed on myeloid cells 2 (TREM2) has been shown with a neuroprotective function against inflammation and neuronal injury in Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

The Alzheimer's disease-associated protective Plcγ2-P522R variant promotes immune functions

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular neurodegeneration 2020-09-11

Microglia-specific genetic variants are enriched in several neurodegenerative diseases, including Alzheimer's disease (AD), implicating a central role for alterations of the innate immune system in the disease etiology. 4 key findings →

Evidence: low

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

Microglia TREM2R47H Alzheimer-linked variant enhances excitatory transmission and reduces LTP via increased TNF-α levels

✓ Peer-reviewed alzhub usefulness score 47 out of 100. eLife 2020-06-24

To study the mechanisms by which the p.R47H variant of the microglia gene and Alzheimer's disease (AD) risk factor TREM2 increases dementia risk, we created Trem2 R47H KI rats. 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

Soluble TREM2 and Inflammatory Proteins in Alzheimer's Disease Cerebrospinal Fluid

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of Alzheimer's disease : JAD 2020-01-01

The present study explores the associations of soluble TREM2, an important regulator of microglial activity linked to Alzheimer's disease (AD), with other known inflammatory proteins in cerebrospinal fluid (CSF). 4 key findings →

Participants: 303 Evidence: low

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

Microglial and peripheral immune priming is partially sexually dimorphic in adolescent mouse offspring exposed to maternal high-fat diet

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of neuroinflammation 2020-09-05

Animal work investigating the consequences of maternal high-fat diet (mHFD) revealed in the offspring a maternal immune activation (MIA) phenotype associated with increased inflammatory signals. 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.

1,034 records (3.6% 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