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Research

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

Find studies

Showing 676–700 of 701 studies in TREM2 and immune genetics (page 28 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.

The triggering receptor expressed on myeloid cells 2: "TREM-ming" the inflammatory component associated with Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Oxidative medicine and cellular longevity 2013-03-06

Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by a progressive loss of memory and cognitive skills. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Functional involvement of γ-secretase in signaling of the triggering receptor expressed on myeloid cells-2 (TREM2)

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of neuroinflammation 2016-01-20

We show that inhibition of γ-secretase-dependent cleavage of the TREM2 C-terminal fragment in cellular membranes interferes with TREM2-dependent signaling and cellular function. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Different mechanisms of apolipoprotein E isoform-dependent modulation of prostaglandin E2 production and triggering receptor expressed on myeloid cells 2 (TREM2) expression after innate immune activation of microglia

✓ Peer-reviewed alzhub usefulness score 38 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2015-01-15

Several lines of evidence support immune response in brain as a mechanism of injury in Alzheimer disease (AD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Immunohistochemical characterization of microglia in Nasu-Hakola disease brains

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neuropathology : official journal of the Japanese Society of Neuropathology 2010-12-01

Nasu-Hakola disease (NHD) is a rare autosomal recessive disorder, characterized by progressive presenile dementia and formation of multifocal bone cysts, caused by genetic mutations of DNAX-activation protein 12 (DAP12) or triggering receptor expressed on myeloid cells 2 (TREM2). 4 key findings →

Evidence: low

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

TREM2 Attenuates Aβ1-42-Mediated Neuroinflammation in BV-2 Cells by Downregulating TLR Signaling

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neurochemical research 2019-05-27

The pathogenesis of late-onset Alzheimer's disease (LOAD) mainly involves abnormal accumulation of extracellular β-amyloid (Aβ) and the consequent neurotoxic effects. 4 key findings →

Evidence: low

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

Expression of the phagocytosis-essential protein TREM2 is down-regulated by an aluminum-induced miRNA-34a in a murine microglial cell line

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of inorganic biochemistry 2013-05-29

One of the key classical pathological features of Alzheimer's disease (AD) is the progressive accumulation of amyloid beta (Aβ42) peptides and their coalescence into highly insoluble senile plaque cores. 4 key findings →

Evidence: low

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

Fluoride activates microglia, secretes inflammatory factors and influences synaptic neuron plasticity in the hippocampus of rats

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Neurotoxicology 2018-09-28

Epidemiological studies have reported that highly fluoridated drinking water may significantly decrease the Intelligence Quotient (IQ) of exposed children. 4 key findings →

Evidence: low

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

Trem2R47H and reduced TREM2 expression both mimic human Alzheimer's disease signatures in mice

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2025-12-19

Trem2*R47H mice had alternative splicing leading to reduced Trem2 expression; Trem2*R47HHSS mice expressed Trem2 at wild-type transcript and protein levels. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Impaired microglial phagocytosis promotes seizure development

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2024-01-02

In the central nervous system, triggering receptor expressed on myeloid cells 2 (TREM2) is exclusively expressed by microglia and is critical for microglial proliferation, migration, and phagocytosis. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Electroacupuncture alleviate cognitive impairment via activation of TREM2-positive microglia in APP/PS1 mice

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-16

EA ameliorated cognitive impairment in APP/PS1 mice by enhancing TREM2⁺ microglia-mediated Aβ clearance and suppressing neuroinflammation. scRNA-seq further revealed that EA reshaped microglial transcriptional states and intercellular communication networks in a TREM2-dependent manner. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

DAP12-deficient microglia adopt a TREM2-independent antigen-presenting state with a glial-to-neuronal cascade in Nasu-Hakola disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-11

Nasu-Hakola disease (NHD), a dementia with about 200 cases worldwide, is caused by loss-of-function mutation of TYROBP , encoding DAP12, or its receptor TREM2 . 5 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

MTHFR*677C>T produces distinct prodromal disease signatures in a mouse model of late-onset Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-09

These data further support the use of the LOAD2.Mthfr 677C>T mouse model to study aspects of ADRD such as cerebrovascular compromise. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Cross-Dataset Reanalysis of Mouse Alzheimer Disease Single-Cell RNA-Sequencing Data Reveals a Reproducible Innate Immune Activation Signature

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-06

Single-cell RNA sequencing (scRNA-seq) studies of Alzheimer’s disease (AD) mouse models have proliferated across independent laboratories, brain regions, and platforms, yet the cross-study reproducibility of transcriptional signatures derived from such data remains underexplored. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

A self-limiting, TREM2-dependent anabolic program confers microglial resilience in Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-20

Microglia are key drivers of Alzheimer’s disease (AD), and TREM2, one of the strongest genetic risk factors, enables the disease-associated microglia (DAM) state required for plaque engagement. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

A sphingomyelin-cholesterol complex regulates TLR4 activation in microglia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-14

Microglial activation in response to lipopolysaccharide (LPS) requires Toll-like receptor 4 (TLR4) redistribution into cholesterol- and sphingolipid-rich membrane domains, yet the lipid determinants of this process remain unclear. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

APOEε4 attenuates early TREM2-mediated microglial responses and influences disease trajectories in dementia with Lewy bodies

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-07-31

Dementia with Lewy bodies (DLB) is characterized by marked biological heterogeneity, only partly explained by the frequent presence of Alzheimer’s disease (AD) copathology. 4 key findings →

Design: longitudinal study Participants: 129 Evidence: moderate

Full summary, score breakdown and related studies → Original source

MicroRNA-223 Enhances Microglia-Dependent Clearance of Amyloid Beta Plaques and Ameliorates Behavioral Deficits in a Mouse Model of Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-23

The Alzheimer’s disease (AD) brain is characterized by dysregulated expression of multiple microRNAs (miRNA), positioning them as promising diagnostic and therapeutic targets. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Immunoproteasome Deficiency Impairs Microglial Clearance and Worsens Tau and Amyloid Pathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-20

Immunoproteasome induction is prominent in Alzheimer’s disease (AD), but whether it protects proteostasis or amplifies neuroinflammation remains unresolved. 2 key findings →

Design: longitudinal study Evidence: moderate

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 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 →

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