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Research

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

Find studies

Showing 951–975 of 1,025 studies in Risk genes beyond APOE (page 39 of 41) · 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 “Risk genes beyond APOE” covers

Risk genes beyond APOE — Genome-wide studies and individual genes other than APOE that shift Alzheimer's risk.

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.

Structure, microtubule interactions, and paired helical filament aggregation by tau mutants of frontotemporal dementias

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Biochemistry 2000-09-01

We have studied biochemical and structural parameters of several missense and deletion mutants of tau protein (G272V, N279K, DeltaK280, P301L, V337M, R406W) found in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Unraveling the conformational landscape of amyloid precursor protein intracellular domain

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Biophysical Journal 2025-08-15

The amyloid precursor protein intracellular domain (AICD), a cleavage product of amyloid precursor protein implicated in Alzheimer disease and amyloid lateral sclerosis, is a functionally important but structurally elusive intrinsically disordered protein. 2 key findings →

Evidence: low

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

γ-Secretase exosites as targets for substrate-selective lowering of Aβ generation

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Structure 2025-12-19

Intramembrane proteolysis by γ-secretase is critically implicated in Alzheimer disease pathogenesis by processing of its amyloid precursor protein substrate C99 into harmful amyloid-β peptide (Aβ) species. 2 key findings →

Evidence: low

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

Activation of neuronal caspase-3 by intracellular accumulation of wild-type Alzheimer amyloid precursor protein

✓ Peer-reviewed alzhub usefulness score 34 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 1999-08-01

Forced overexpression of wild-type Alzheimer amyloid precursor protein (APP) causes postmitotic neurons to degenerate. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Evaluating the impact of age and treatment on neuroinflammation-related proteins in mouse models of proteinopathies

✓ Peer-reviewed alzhub usefulness score 34 out of 100. Experimental Neurology 2025-09-22

Neuroinflammation plays a key role in Alzheimer's disease (AD), but the actions of microglial mediators may vary across stages of Aβ pathology. 1 key finding →

Evidence: low

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

A Novel TREM2 Small Molecule Agonist MTX46943 Re‐Programs Human Microglia and Reduces Amyloid Pathology In Vivo

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Alzheimer s & Dementia 2025-12-01

MTX46943-mediated TREM2 activation leads to TREM2/DAP12 receptor complex formation and stabilizes surface location required for downstream signaling and microglia activation. 5 key findings →

Evidence: low

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

Developments on BACE 1 Inhibitors as Anti‐Alzheimer Agents: A Perspective on Medicinal Chemistry‐Based Advances

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Archiv der Pharmazie 2026-03-01

Alzheimer's disease (AD) is a progressive and complicated neurodegenerative disorder that mostly affects the elderly and is characterized by memory loss, cognitive dysfunction, accumulation of amyloid beta (Aβ) plaques, neurofibrillary tangles, and cholinergic deficits. 1 key finding →

Evidence: low

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

Quantitative EEG obtained from Dual‐Task paradigms for the study of preclinical populations at risk of Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Alzheimer s & Dementia 2025-12-01

The most notable effect sizes were observed in entropy for Beta1 and Beta3 bands in frontal regions for the DTS7 and DTS1 tasks, Beta2 relative power in C4 during DTAN, Theta modulation in the Theta and alpha-1 bands in frontal regions during DTS7, and Alpha2 modulations in the same task. 5 key findings →

Participants: 37 Evidence: low

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

Quantitative EEG obtained from Dual‐Task paradigms for the study of preclinical populations at risk of Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Alzheimer s & Dementia 2025-12-01

The most notable effect sizes were observed in entropy for Beta1 and Beta3 bands in frontal regions for the DTS7 and DTS1 tasks, Beta2 relative power in C4 during DTAN, Theta modulation in the Theta and alpha-1 bands in frontal regions during DTS7, and Alpha2 modulations in the same task. 5 key findings →

Participants: 37 Evidence: low

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

Cytoplasmic expression of trans-active response DNA-binding protein-43 in aged mice display hippocampal sclerosis-like degeneration and neuronal loss with reduced lifespan

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Journal of Neuropathology & Experimental Neurology 2025-01-26

Trans-active response DNA-binding protein-43 (TDP-43) is the major pathological protein in motor neuron disease and TDP-43 pathology has been described in the brains of up to 50% of patients with Alzheimer disease (AD). 5 key findings →

Evidence: low

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

Splenomegaly, Spleen Amyloidosis and Neutrophil Infiltration are Present in 3xTg-AD, but not Tg-SwDI Mice

✓ Peer-reviewed alzhub usefulness score 33 out of 100. NeuroMolecular Medicine 2025-09-04

It is now widely accepted that the development of neurodegenerative diseases depends on and affects many pathological processes, both in the brain and the periphery. 1 key finding →

Evidence: low

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

Network-based gene prioritization using hybrid scoring for complex disease module discovery

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Scientific Reports 2026-09-19

In each case the framework recovered known disease genes and identified biologically coherent, disease-specific modules: in AD, 17 stable high-confidence genes and modules enriched in lipid and cholesterol metabolism and amyloid precursor protein processing; in PD, 17 stable genes and modules associated with mitophagy, ubiquitin-proteasome signaling, and mitochondrial dysfunction; in RA, 20 stable genes and modules enriched in antigen presentation and JAK-STAT cytokine signaling. 2 key findings →

Evidence: low

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

Cryo‐EM structures of amyloid β filaments from cotton wool plaques in Alzheimer disease caused by the PSEN1 V261I and A431E mutations

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Alzheimer s & Dementia 2025-12-01

CWPs consist predominantly of two novel arrangements of type I Aβ filaments, and we have designated them as type Ic and type Id Aβ filaments. 5 key findings →

Evidence: low

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

Neurophysiological markers of cholinergic dysfunction in pre‐symptomatic autosomal dominant Alzheimer´s disease using Transcranial Magnetic Stimulation (TMS): research design and preliminary results

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Alzheimer s & Dementia 2025-12-01

Here we present our research design and preliminary results in ADAD mutation carriers and controls. 5 key findings →

Evidence: low

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

[Screening for mutations of the precursor of beta-amyloid protein in early forms of Alzheimer disease. French Study Group of Alzheimer Disease]

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Revue neurologique 1993-01-01

Genetic linkage studies suggest that Alzheimer's disease (AD) is genetically heterogeneous and that in several early onset families the disease locus is close to the amyloid precursor protein (APP) gene on chromosome 21. 2 key findings →

Design: clinical trial Evidence: low

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

Single-cell atlas reveals pathological amplification of aging programs and proteostasis collapse in microglia of Alzheimer′s disease mice

✓ Peer-reviewed alzhub usefulness score 30 out of 100. DOAJ (DOAJ: Directory of Open Access Journals) 2026-06-01

The pathological activation of AD microglia significantly amplifies endogenous aging characteristics. 4 key findings →

Evidence: low

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

Presenilin 1 M139I mutation regulates the microRNA-34a-mediated neurogenic locus notch homolog protein 1 signaling pathway in an early-onset Alzheimer disease cell model

✓ Peer-reviewed alzhub usefulness score 30 out of 100. Journal of Neuropathology & Experimental Neurology 2025-04-26

Presenilin 1 (PSEN1) mutations are the leading cause of early-onset Alzheimer disease (EOAD). 3 key findings →

Evidence: low

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

Combating cognitive decline in a rat model of Alzheimer’s disease: The role of high-intensity interval training and cannabidiol administration in modulating microRNA-124, BACE1, and nestin

✓ Peer-reviewed alzhub usefulness score 30 out of 100. Current Journal of Neurology 2026-05-30

HIIT alone and in combination with CBD treatment significantly improved cognitive impairment induced by 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. 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