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Research

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

Find studies

Showing 26–50 of 301 studies · free to read (page 2 of 13) · 29,780 in the whole library · How the 0–100 score works

Download bibliography of these 301 studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 301 studies tagged soluble — clear

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

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.

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.

sTREM2 cerebrospinal fluid levels are a potential biomarker for microglia activity in early-stage Alzheimer's disease and associate with neuronal injury markers

✓ Peer-reviewed alzhub usefulness score 60 out of 100. EMBO molecular medicine 2016-05-02

TREM2 is an innate immune receptor expressed on the surface of microglia. 4 key findings →

Design: cross-sectional Evidence: low

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

Increased cerebrospinal fluid soluble TREM2 concentration in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Molecular neurodegeneration 2016-01-12

The discovery that heterozygous missense mutations in the gene encoding triggering receptor expressed on myeloid cells 2 (TREM2) are risk factors for Alzheimer's disease (AD), with only the apolipoprotein E (APOE) ε4 gene allele conferring a higher risk, has led to increased interest in immune biology in the brain. 4 key findings →

Participants: 37 Evidence: moderate

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

Mechanism of STMN2 cryptic splice-polyadenylation and its correction for TDP-43 proteinopathies

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Science (New York, N.Y.) 2023-03-16

Loss of nuclear TDP-43 is a hallmark of neurodegeneration in TDP-43 proteinopathies, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 4 key findings →

Evidence: low

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

TREM2 Maintains Microglial Metabolic Fitness in Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Cell 2017-08-01

Elevated risk of developing Alzheimer's disease (AD) is associated with hypomorphic variants of TREM2, a surface receptor required for microglial responses to neurodegeneration, including proliferation, survival, clustering, and phagocytosis. 4 key findings →

Evidence: low

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

Soluble TREM2 is elevated in Parkinson's disease subgroups with increased CSF tau

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Brain : a journal of neurology 2020-03-01

Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease and affects 1% of the population above 60 years old. 4 key findings →

Design: cross-sectional Participants: 165 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

TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer's disease mouse models

✓ Peer-reviewed alzhub usefulness score 58 out of 100. The Journal of experimental medicine 2015-03-02

Variants in triggering receptor expressed on myeloid cells 2 (TREM2) confer high risk for Alzheimer's disease (AD) and other neurodegenerative diseases. 4 key findings →

Evidence: low

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

TREM2 activation on microglia promotes myelin debris clearance and remyelination in a model of multiple sclerosis

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Acta neuropathologica 2020-08-09

Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) triggered by autoimmune mechanisms. 4 key findings →

Evidence: low

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

Using exome sequencing to reveal mutations in TREM2 presenting as a frontotemporal dementia-like syndrome without bone involvement

✓ Peer-reviewed alzhub usefulness score 57 out of 100. JAMA neurology 2013-01-01

Our results show that TREM2 is responsible for an unexpectedly high number of dementia cases in our cohort, suggesting that this gene should be taken into account when mutations in other dementia genes are excluded. 4 key findings →

Evidence: moderate

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

TREM2 Haplodeficiency in Mice and Humans Impairs the Microglia Barrier Function Leading to Decreased Amyloid Compaction and Severe Axonal Dystrophy

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neuron 2016-05-01

Haplodeficiency of the microglia gene TREM2 increases risk for late-onset Alzheimer's disease (AD) but the mechanisms remain uncertain. 4 key findings →

Evidence: low

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

The Microglial Innate Immune Receptor TREM2 Is Required for Synapse Elimination and Normal Brain Connectivity

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Immunity 2018-05-08

The triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial innate immune receptor associated with a lethal form of early, progressive dementia, Nasu-Hakola disease, and with an increased risk of Alzheimer's disease. 4 key findings →

Evidence: low

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

Soluble TREM2 ameliorates pathological phenotypes by modulating microglial functions in an Alzheimer's disease model

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Nature communications 2019-03-25

Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial surface receptor genetically linked to the risk for Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

Heterozygous TREM2 mutations in frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neurobiology of aging 2013-10-16

A causative association was recently demonstrated between homozygous TREM2 mutations and frontotemporal dementia (FTD)-like syndrome and between heterozygous TREM2 exon2 genetic variations and late-onset Alzheimer's disease (AD). 4 key findings →

Participants: 1,030 Evidence: low

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

Increased DNA methylation near TREM2 is consistently seen in the superior temporal gyrus in Alzheimer's disease brain

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neurobiology of aging 2016-07-16

Although mutations within the TREM2 gene have been robustly associated with Alzheimer's disease, it is not known whether alterations in the regulation of this gene are also involved in pathogenesis. 3 key findings →

Design: meta-analysis Evidence: high

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

sTREM2 is associated with amyloid-related p-tau increases and glucose hypermetabolism in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. EMBO molecular medicine 2023-01-09

Microglial activation occurs early in Alzheimer's disease (AD) and previous studies reported both detrimental and protective effects of microglia on AD progression. 4 key findings →

Design: cross-sectional Participants: 70 Evidence: moderate

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

Cerebrospinal fluid soluble TREM2 levels in frontotemporal dementia differ by genetic and pathological subgroup

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Alzheimer's research & therapy 2018-08-16

Reliable biomarkers of frontotemporal dementia (FTD) are currently lacking. 4 key findings →

Design: longitudinal study Participants: 20 Evidence: moderate

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

TREM2 deficiency impairs chemotaxis and microglial responses to neuronal injury

✓ Peer-reviewed alzhub usefulness score 56 out of 100. EMBO reports 2017-05-08

Sequence variations in the triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to an increased risk for neurodegenerative disorders such as Alzheimer's disease and frontotemporal lobar degeneration. 2 key findings →

Evidence: low

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

TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2017-10-09

Variants in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) were recently found to increase the risk for developing Alzheimer's disease (AD). 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.

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