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Research

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

Find studies

Showing 251–275 of 363 studies (page 11 of 15) · 27,380 in the whole library · How the 0–100 score works

Showing 363 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; 12,859 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.

The surface-exposed chaperone, Hsp60, is an agonist of the microglial TREM2 receptor

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Journal of neurochemistry 2009-04-29

Triggering receptor expressed in myeloid (TREM) cells 2, a receptor expressed by myeloid cells, osteoclasts and microglia, is known to play a protective role in bones and brain. 4 key findings →

Evidence: low

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

Microglia-Mediated Neuroprotection, TREM2, and Alzheimer's Disease: Evidence From Optical Imaging

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Biological psychiatry 2017-10-14

Recent genetic studies have provided overwhelming evidence of the involvement of microglia-related molecular networks in the pathophysiology of Alzheimer's disease (AD). 4 key findings →

Evidence: low

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

TREM2 promotes Aβ phagocytosis by upregulating C/EBPα-dependent CD36 expression in microglia

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Scientific reports 2017-09-11

TREM2 plays a critical role in the alleviation of Alzheimer's disease by promoting Aβ phagocytosis by microglia, but the detailed molecular mechanism underlying TREM2-induced direct phagocytic activity of Aβ remains to be revealed. 4 key findings →

Evidence: low

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

Distinct Signaling Pathways Regulate TREM2 Phagocytic and NFκB Antagonistic Activities

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Frontiers in cellular neuroscience 2019-10-10

Several genetic variants of the Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) have been shown to increase the risk of developing Alzheimer's disease (AD) supporting a role of microglia and immune cells in the pathobiology of AD. 4 key findings →

Evidence: low

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

Immunosuppressive TREM2(+) macrophages are associated with undesirable prognosis and responses to anti-PD-1 immunotherapy in non-small cell lung cancer

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Cancer immunology, immunotherapy : CII 2022-03-12

Immune checkpoint blockade (ICB) has been improving patient outcomes of non-small cell lung cancer (NSCLC), but its effectiveness is highly subjective to individual tumor microenvironment. 4 key findings →

Evidence: low

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

TREM2-Dependent Effects on Microglia in Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Frontiers in aging neuroscience 2018-07-09

Alzheimer's disease (AD) is a late-onset dementia characterized by the deposition of amyloid plaques and formation of neurofibrillary tangles (NFTs) which lead to neuronal loss and cognitive deficits. 4 key findings →

Evidence: low

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

Human stem cell-derived monocytes and microglia-like cells reveal impaired amyloid plaque clearance upon heterozygous or homozygous loss of TREM2

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2018-11-12

Murine microglia expressing the Alzheimer's disease-linked TREM2 R47H mutation display variable decrease in phagocytosis, while impaired phagocytosis is reported following loss of TREM2. 4 key findings →

Evidence: low

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

Microglia, Trem2, and Neurodegeneration

✓ Peer-reviewed alzhub usefulness score 46 out of 100. The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry 2024-05-20

Microglia are a specialized type of neuroimmune cells that undergo morphological and molecular changes through multiple signaling pathways in response to pathological protein aggregates, neuronal death, tissue injury, or infections. 4 key findings →

Evidence: low

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

TREM2 variants that cause early dementia and increase Alzheimer's disease risk affect gene splicing

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain 2024-01-16

This molecular genetics study found that several TREM2 gene variants previously thought to work only by altering the TREM2 protein itself, also disrupt how the TREM2 gene's RNA message is spliced together, sometimes producing dysfunctional protein versions. 4 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

TREM2 inhibits inflammatory responses in mouse microglia by suppressing the PI3K/NF-κB signaling

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Cell biology international 2018-05-10

This study aimed to investigate the effects of triggering receptor expressed on myeloid cell-2 (TREM2) on the production of pro-inflammatory mediators and cytokines induced by lipopolysaccharide (LPS) in BV2 microglia. 4 key findings →

Evidence: low

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

Distribution and signaling of TREM2/DAP12, the receptor system mutated in human polycystic lipomembraneous osteodysplasia with sclerosing leukoencephalopathy dementia

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The European journal of neuroscience 2004-11-01

Together with its adaptor protein, the adaptor protein of 12 kDa also known as KARAP and TYROBP (DAP12), triggering receptor expressed in myeloid cells 2 (TREM2) is a stimulatory membrane receptor of the immunoglobulin/lectin-like superfamily, well known in myeloid cells. 4 key findings →

Evidence: low

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

TREM2 Protein Expression Changes Correlate with Alzheimer's Disease Neurodegenerative Pathologies in Post-Mortem Temporal Cortices

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain pathology (Zurich, Switzerland) 2014-11-11

Triggering receptor expressed by myeloid cells 2 (TREM2), a member of the immunoglobulin superfamily, has anti-inflammatory phagocytic function in myeloid cells. 4 key findings →

Evidence: low

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

TREM2 Function in Alzheimer's Disease and Neurodegeneration

✓ Peer-reviewed alzhub usefulness score 45 out of 100. ACS chemical neuroscience 2016-02-19

Alzheimer's disease (AD), the most common cause of dementia in the elderly, is a complex neurodegenerative disease marked by the appearance of amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles. 4 key findings →

Evidence: low

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

TREM2-activating antibodies abrogate the negative pleiotropic effects of the Alzheimer's disease variant Trem2R47H on murine myeloid cell function

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2018-03-29

Triggering receptor expressed on myeloid cells 2 (TREM2) is an orphan immune receptor expressed on cells of myeloid lineage such as macrophages and microglia. 4 key findings →

Evidence: low

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

The triggering receptor expressed on myeloid cells 2 (TREM2) is associated with enhanced inflammation, neuropathological lesions and increased risk for Alzheimer's dementia

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2014-12-09

The TREM2 variant is associated with: (i) AD (odds ratio: 4.76; P = .014); (ii) increased density of amyloid plaques and neurofibrillary tangles in multiple brain regions; (iii) increased TREM2 (P = .041) and TYROBP (P = .006) gene expression; (iv) decreased TREM2 protein levels (P = .016); and (v) upregulation of proinflammatory cytokines (regulated on activation, norma 3 key findings →

Evidence: low

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

TREM2-induced activation of microglia contributes to synaptic integrity in cognitively intact aged individuals with Alzheimer's neuropathology

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain pathology (Zurich, Switzerland) 2022-07-11

The existence of individuals who remain cognitively intact despite presenting histopathological signs of Alzheimer's disease (AD), here referred to as "Nondemented with AD neuropathology" (NDAN), suggests that some mechanisms are triggered to resist cognitive impairment. 4 key findings →

Evidence: low

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

From across this tag

8 of the 363 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 8. The same 8 appear here every time.

↑ Change the filters

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 →

Newest studies, as a dated timeline →    Atom feed