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Research

29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 376–400 of 448 studies in Risk genes beyond APOE · free to read (page 16 of 18) · 29,380 in the whole library · How the 0–100 score works

Download bibliography of these 448 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; 14,855 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.

Downregulated miR-29c correlates with increased BACE1 expression in sporadic Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 39 out of 100. International journal of clinical and experimental pathology 2015-02-01

Beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1) is conceived as a potential target for therapies against Alzheimer disease (AD) which is characterized by the accumulation of plaques formed of short β-amyloid (APPβ) peptides. 4 key findings →

Evidence: low

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

Treatment strategies targeting amyloid β-protein

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cold Spring Harbor perspectives in medicine 2012-09-01

With the advent of the key discovery in the mid-1980s that the amyloid β-protein (Aβ) is the core constituent of the amyloid plaque pathology found in Alzheimer disease (AD), an intensive effort has been underway to attempt to mitigate its role in the hope of treating the disease. 3 key findings →

Evidence: low

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

Engineered butyrate-producing yeasts mitigate Alzheimer-associated phenotypes

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Signal Transduction and Targeted Therapy 2025-11-16

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease without effective treatments. 1 Extracellular amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss are the characteristics of AD neuropathology. 4 key findings →

Evidence: low

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

Alzheimer-mutant γ-secretase complexes stall amyloid β-peptide production

✓ Peer-reviewed alzhub usefulness score 39 out of 100. eLife 2025-02-11

Missense mutations in the amyloid precursor protein (APP) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer’s disease (FAD) and alter proteolytic production of secreted 38-to-43-residue amyloid β-peptides (Aβ) by the PSEN1-containing γ-secretase complex, ostensibly supporting the amyloid hypothesis of pathogenesis. 3 key findings →

Evidence: low

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

TBG096 Ameliorates Memory Deficiency in AD Mouse Model via Promoting Neurogenesis and Regulation of Hsc70/HK2/PKM2/LAMP2A Signaling Pathway

✓ Peer-reviewed alzhub usefulness score 39 out of 100. International Journal of Molecular Sciences 2025-03-20

In previous studies, we isolated a series of novel gentisides with nerve growth factor (NGF)-mimic activities from Gentiana rigescens Franch and conducted continuous structure–activity relationship (SAR) studies. 5 key findings →

Evidence: low

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

Low CSF APP refines diagnosis for p ‐tau negative Alzheimer‐like dementia

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia 2025-12-01

Concentrations of CSF APP were significantly lower in T- compared to T+ individuals across all clinical diagnostic groups across cohorts, regardless of A± status (Figure 1). 5 key findings →

Participants: 384 Evidence: low

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

Novel fully human high-affinity anti-TREM2 antibody shows efficacy in clinically relevant Alzheimer´s mouse model

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Alzheimer s Research & Therapy 2025-05-22

M07-TFN showed higher binding affinities and stronger activation of hTREM2 signaling than all previously described anti-hTREM2 antibodies. p-Syk activation was increased 30-fold in hTREM2-overexpressing HEK293 cells and fourfold in human microglia cells compared to baseline. 5 key findings →

Evidence: low

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

The connection between autophagy and Alzheimer’s disease

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Inflammation Research 2025-10-22

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease associated with accumulation of amyloid beta peptides and intracellular neurofibrillary tangles formed by hyperphosphorylated Tau. 1 key finding →

Evidence: low

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

Genetic association of ABCA7 and PSEN1 polymorphisms with Alzheimer’s disease in the northeast Algerian population: Exploring risk factors

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Archives of Biological Sciences 2025-01-01

Alzheimer?s disease (AD) is a neurodegenerative disorder with a strong genetic component. 4 key findings →

Design: case-control study Participants: 98 Evidence: moderate

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

APP‐mediated intracellular signaling rescues sleep impairment and blood–brain barrier leakage in Alzheimer's disease mouse model

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Alzheimer s & Dementia 2026-02-01

APP‐mediated signaling plays a key role in regulating sleep, maintaining BBB integrity, and preserving memory in AD. 1 key finding →

Evidence: low

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

Effect of epigallocatechin-3-gallate (EGCG) on cognitive functioning and the expression of APP and BDNF in the hippocampus of rats with streptozotocin -induced Alzheimer-like disease

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Biochemistry and Biophysics Reports 2025-01-31

We aimed to investigate the potential therapeutic effects of the active substance of green tea, epigallocatechin-3-gallate (EGCG), on behavioral phenotypes and markers of neurogenesis in an Alzheimer disease (AD) rat model. 4 key findings →

Evidence: low

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

HIF‐1 Targeting Intervention Renders Protection From Alzheimer's‐Like Pathology in a Humanized Mice Model of HIV Infection

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of Extracellular Vesicles 2025-11-01

HIV-associated neurocognitive disorders (HAND) affect 30%-50% of individuals living with HIV on combination antiretroviral therapy, with Alzheimer 's-like pathology as a potent comorbidity of HAND. 2 key findings →

Evidence: low

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

Cerebral FURIN deficiency impairs astrocytic lipophagy through ITGAV maturation

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Autophagy 2025-12-11

: ACTB: actin, beta; AD: Alzheimer disease; ADAM10: a disintegrin and metallopeptidase domain 10; ADGGA: acyl diacylglyceryl glucuronide; AHexSIS: acylhexosyl sitosterol; AHexSTS: acylhexosyl stigmasterol; AIF1/IBA1: allograft inflammatory factor 1; APP: amyloid beta precursor protein; ATG5: autophagy related 5; Aβ: amyloid β-protein; BACE1: beta-site APP cleaving enzyme 1; BASulfate: bile acid sulfate; BMP: bismonoacylglycerophosphate; CAR: acylcarnitine; CE: cholesteryl ester; Cer_NS: ceramide non-hydroxyfatty acid-sphingosine; CL: cardiolipin; CMA: chaperone-mediated autophagy; DAPI: 4',6-diamidino-2-phenylindole; DCAE: esterified deoxycholic acid; DEP: differentially expressed protein; DG: diacylglycerol; DGCC: diacylglyceryl-3-O-carboxyhydroxymethylcholine; DLG4/PSD95: discs large MAGUK scaffold protein 4; ECM: extracellular matrix; EtherLPC: ether-linked lysophosphatidylcholine; EtherLPE: ether-linked lysophosphatidylethanolamine; EtherMGDG: ether-linked monogalactosyldiacylglycerol; EtherOxPC: ether-linked oxidized phosphatidylcholine; EtherPC: ether-linked phosphatidylcholine; EtherPE: ether-linked phosphatidylethanolamine; EtherPG: ether-linked phosphatidylglycerol; EtherSMGDG: semino lipid; EtherTG: ether-linked triacylglycerol; FA: fatty acyls; FA: free fatty acid; FAHFA: fatty acid ester of hydroxyl fatty acid; FJC: fluoro-Jade C; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GDCAE: esterified glycodeoxycholic acid; GFAP: glial fibrillary acidic protein; GL: glycerolipids; GP: glycerophospholipids; HBMP: hemibismonoacylglycerophosphate; HexCer_NS: hexosylceramide non-hydroxyfatty acid-sphingosine; HSPA8/HSC70: heat shock protein 8; IP-MS: immunoprecipitation-mass spectrometry; KEGG: Kyoto Encyclopedia of Genes and Genomes; LAMP1: lysosomal-associated membrane protein 1; LAMP2A: lysosomal-associated membrane protein 2A; LDGCC: lysodiacylglyceryl-3-O-carboxyhydroxymethylcholine; LDs: lipid droplets; LNAPE: N-acyl-lysophosphatidylethanolamine; LNAPS: N-acyl-lysophosphatidylserine; LPA: lysophosphatidic acid; LPC: lyso-phophatidylcholine; LPE: lysophosphatidylethanolamine; LPG: lysophosphatidylglycerol; LPI: lysophosphatidylinositol; LPS: lysophosphatidylserine; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MGDG: monogalactosyldiacylglycerol; MWM: Morris Water Maze; OA: oleic acid; OFT: Open Field Test; OxPC: oxidized phosphatidylcholine; OxPG: oxidized phosphatidylglycerol; OxPI: oxidized phosphatidylinositol; OxPS: oxidiz 1 key finding →

Evidence: low

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

Characterization of endothelin-converting enzyme 1 as a key enzyme in the multienzyme Aβ degradation pathway

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences 2025-10-27

Altered β-amyloid (Aβ) homeostasis is a critical event triggering the shift from healthy aging to Alzheimer disease (AD) through the overproduction and impaired clearance of Aβ peptides. 2 key findings →

Evidence: low

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

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

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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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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