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Research

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

Find studies

Showing 7,626–7,650 of 10,985 studies · free to read (page 306 of 440) · 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.

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.

γ-Secretase modulator (GSM) photoaffinity probes reveal distinct allosteric binding sites on presenilin

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2013-02-08

γ-Secretase is an intramembrane aspartyl protease that cleaves the amyloid precursor protein to produce neurotoxic β-amyloid peptides (i.e. Aβ42) that have been implicated in the pathogenesis of Alzheimer disease. 4 key findings →

Evidence: low

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

Generation of Alzheimer disease-associated amyloid β42/43 peptide by γ-secretase can be inhibited directly by modulation of membrane thickness

✓ Peer-reviewed alzhub usefulness score 44 out of 100. The Journal of biological chemistry 2012-04-24

Pathogenic generation of amyloid β-peptide (Aβ) by sequential cleavage of β-amyloid precursor protein (APP) by β- and γ-secretases is widely believed to causally underlie Alzheimer disease (AD). β-Secretase initially cleaves APP thereby generating a membrane-bound APP C-terminal fragment, from which γ-secretase subsequently liberates 37-43-amino acid long Aβ species. 4 key findings →

Evidence: low

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

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

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

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

Microglia influence host defense, disease, and repair following murine coronavirus infection of the central nervous system

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Glia 2020-05-25

The present study examines functional contributions of microglia in host defense, demyelination, and remyelination following infection of susceptible mice with a neurotropic coronavirus. 4 key findings →

Evidence: low

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

TREM2 mediates physical exercise-promoted neural functional recovery in rats with ischemic stroke via microglia-promoted white matter repair

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neuroinflammation 2023-02-25

The repair of white matter injury is of significant importance for functional recovery after ischemic stroke, and the up-regulation of triggering receptors expressed on myeloid cells 2 (TREM2) after ischemic stroke is neuroprotective and implicated in remyelination. 4 key findings →

Evidence: low

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

Triggering receptor expressed on myeloid cells-2 expression in the brain is required for maximal phagocytic activity and improved neurological outcomes following experimental stroke

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 2018-12-07

Triggering receptor expressed on myeloid cells-2 (TREM2) is an innate immune receptor that promotes phagocytosis by myeloid cells such as microglia and macrophages. 4 key findings →

Evidence: low

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

A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Molecular neurodegeneration 2023-02-17

Unfortunately, many current Trem2 R47H mouse models are associated with cryptic mRNA splicing of the mutant allele that produces a confounding reduction in protein product. 4 key findings →

Evidence: low

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

Models of microglia depletion and replenishment elicit protective effects to alleviate vascular and neuronal damage in the diabetic murine retina

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of neuroinflammation 2022-12-14

Microglia, the resident phagocytes of the retina, are believed to influence the development of retinopathy, but their exact contributions to vascular integrity and neuronal loss are unknown. 4 key findings →

Evidence: low

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

↑ 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.

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