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Research

29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 501–525 of 824 studies in TREM2 and immune genetics marked Peer-reviewed (page 21 of 33) · 29,780 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these 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; 15,255 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.

Essential role of the microglial triggering receptor expressed on myeloid cells-2 (TREM2) for central nervous tissue immune homeostasis

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neuroimmunology 2007-01-18

While there is a strong evidence for neural tissue destruction mediated by adaptive autoimmune responses, it is still debated how innate immune responses contribute to neuroinflammatory and neurodegenerative diseases such as multiple sclerosis and Alzheimer's disease. 4 key findings →

Evidence: low

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

Targeting microglia for the treatment of Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Glia 2016-04-21

While histological changes in microglia have long been recognized as a pathological feature of Alzheimer's disease (AD), recent genetic association studies have also strongly implicated microglia in the etiology of the disease. 3 key findings →

Evidence: low

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

TREM2, a DAP12-associated receptor, regulates osteoclast differentiation and function

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2005-10-20

These results provide new evidence that TREM2 regulates OC function independent of its effects on multinucleated OC differentiation. 4 key findings →

Evidence: low

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

Convergence between Microglia and Peripheral Macrophages Phenotype during Development and Neuroinflammation

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2019-12-09

Differently from other myeloid cells, microglia derive exclusively from precursors originating within the yolk sac and migrate to the CNS under development, without any contribution from fetal liver or postnatal hematopoiesis. 4 key findings →

Evidence: low

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

Systematic Pan-Cancer Analysis Identifies TREM2 as an Immunological and Prognostic Biomarker

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Frontiers in immunology 2021-02-17

Triggering receptor expressed on myeloid cells-2 (TREM2) is a transmembrane receptor of the immunoglobulin superfamily and a crucial signaling hub for multiple pathological pathways that mediate immunity. 4 key findings →

Evidence: low

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

TREM2 overexpression rescues cognitive deficits in APP/PS1 transgenic mice by reducing neuroinflammation via the JAK/STAT/SOCS signaling pathway

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Experimental neurology 2020-10-13

Overactivated microglia and neuroinflammation are considered to play a crucial role in the progression of Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

TREM2 in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Molecular neurobiology 2013-02-14

Recent works have demonstrated a rare functional variant (R47H) in triggering receptor expressed on myeloid cells (TREM) 2 gene, encoding TREM2 protein, increase susceptibility to late-onset Alzheimer's disease (AD), with an odds ratio similar to that of the apolipoprotein E ε4 allele. 4 key findings →

Evidence: low

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

Negative regulation of TLR signaling in myeloid cells--implications for autoimmune diseases

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Immunological reviews 2016-01-01

Toll-like receptors (TLR) are transmembrane pattern recognition receptors that recognize microbial ligands and signal for production of inflammatory cytokines and type I interferon in macrophages and dendritic cells (DC). 4 key findings →

Evidence: low

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

Extracellular signal-regulated kinase regulates microglial immune responses in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neuroscience research 2021-03-17

The importance of mitogen-activated protein kinase (MAPK) pathway signaling in regulating microglia-mediated neuroinflammation in Alzheimer's disease (AD) remains unclear. 4 key findings →

Evidence: low

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

Triggering Receptor Expressed on Myeloid Cells 2 Deficiency Alters Acute Macrophage Distribution and Improves Recovery after Traumatic Brain Injury

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neurotrauma 2016-05-09

Traumatic brain injury (TBI) affects 1.7 million persons annually in the United States (Centers for Disease Control and Prevention). 4 key findings →

Evidence: low

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

TREM2-independent oligodendrocyte, astrocyte, and T cell responses to tau and amyloid pathology in mouse models of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Cell reports 2021-12-01

Non-neuronal responses in neurodegenerative disease have received increasing attention as important contributors to disease pathogenesis and progression. 4 key findings →

Evidence: low

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

Elevated microglial oxidative phosphorylation and phagocytosis stimulate post-stroke brain remodeling and cognitive function recovery in mice

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Communications biology 2022-01-11

New research shows that disease-associated microglia in neurodegenerative brains present features of elevated phagocytosis, lysosomal functions, and lipid metabolism, which benefit brain repair. 4 key findings →

Evidence: low

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

Cyanidin-3-O-Glucoside Regulates the M1/M2 Polarization of Microglia via PPARγ and Aβ42 Phagocytosis Through TREM2 in an Alzheimer's Disease Model

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Molecular neurobiology 2022-06-07

Microglial polarization plays an essential role in the progression and regression of neurodegenerative disorders. 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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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 (3.5% 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