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Research

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

Find studies

Showing 1–25 of 57 studies with an author at Institute Born-Bunge (BE) (page 1 of 3) · 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.

Other 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.

Genetic meta-analysis of diagnosed Alzheimer's disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing

✓ Peer-reviewed alzhub usefulness score 85 out of 100. Nature genetics 2019-02-28

Risk for late-onset Alzheimer's disease (LOAD), the most prevalent dementia, is partially driven by genetics. 5 key findings →

Design: meta-analysis Participants: 94,437 Evidence: high

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

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 82 out of 100. Nature genetics 2017-07-17

We identified rare coding variants associated with Alzheimer's disease in a three-stage case-control study of 85,133 subjects. 4 key findings →

Design: case-control study Participants: 85,133 Evidence: moderate

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

Frontotemporal dementia and its subtypes: a genome-wide association study

✓ Peer-reviewed alzhub usefulness score 78 out of 100. The Lancet. Neurology 2014-07-01

Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. 4 key findings →

Design: meta-analysis Participants: 3,526 Evidence: high

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

Increased expression of BIN1 mediates Alzheimer genetic risk by modulating tau pathology

✓ Peer-reviewed alzhub usefulness score 72 out of 100. Molecular psychiatry 2013-02-12

Genome-wide association studies (GWAS) have identified a region upstream the BIN1 gene as the most important genetic susceptibility locus in Alzheimer's disease (AD) after APOE. 1 key finding →

Design: meta-analysis Evidence: high

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

Diagnostic Value of Cerebrospinal Fluid Neurofilament Light Protein in Neurology: A Systematic Review and Meta-analysis

✓ Peer-reviewed alzhub usefulness score 69 out of 100. JAMA neurology 2019-09-01

These data support the use of cNfL as a biomarker of neuroaxonal damage and indicate that age-specific and sex-specific (and in some cases disease-specific) reference values may be needed. 4 key findings →

Participants: 2,795 Evidence: moderate

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

Both common variations and rare non-synonymous substitutions and small insertion/deletions in CLU are associated with increased Alzheimer risk

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Molecular neurodegeneration 2012-01-16

We identified a new genetic risk association of AD with rare coding CLU variations that is independent of the 5' common association signal identified in the GWA studies. 3 key findings →

Design: meta-analysis Participants: 1,930 Evidence: high

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

Association of Rare APOE Missense Variants V236E and R251G With Risk of Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 67 out of 100. JAMA neurology 2022-07-01

In this genetic association study, a novel variant associated with AD was identified: R251G always coinherited with ε4 on the APOE gene, which mitigates the ε4-associated AD risk. 5 key findings →

Design: case-control study Participants: 37 Evidence: moderate

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

New insights into the genetic etiology of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Nature genetics 2022-04-04

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. 2 key findings →

Evidence: low

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

Age and the association between apolipoprotein E genotype and Alzheimer disease: A cerebrospinal fluid biomarker-based case-control study

✓ Peer-reviewed alzhub usefulness score 66 out of 100. PLoS medicine 2020-08-20

The ε4 allele of apolipoprotein E (APOE) gene and increasing age are two of the most important known risk factors for developing Alzheimer disease (AD). 4 key findings →

Design: cohort study Participants: 1,593 Evidence: moderate

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

Advancing research diagnostic criteria for Alzheimer's disease: the IWG-2 criteria

✓ Peer-reviewed alzhub usefulness score 66 out of 100. The Lancet Neurology 2014-05-18

This Position Paper evaluates the strengths and limitations of the International Working Group research diagnostic criteria and proposes advances to improve the diagnostic framework for Alzheimer's disease.

Evidence: low

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

Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Nature Genetics 2011-04-03

The authors sought to identify new susceptibility loci for Alzheimer's disease through a staged association study and by testing suggestive loci reported by the Alzheimer's Disease Genetic Consortium in a companion paper. 2 key findings →

Evidence: low

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

Alzheimer risk associated with a copy number variation in the complement receptor 1 increasing C3b/C4b binding sites

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Molecular psychiatry 2011-03-15

Two multicentre genome-wide association (GWA) studies provided substantial evidence, implicating the complement receptor 1 gene (CR1) in Alzheimer disease (AD) genetic etiology. 3 key findings →

Participants: 1,883 Evidence: moderate

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

Null mutations in progranulin cause ubiquitin-positive frontotemporal dementia linked to chromosome 17q21

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 2006-07-16

Frontotemporal dementia (FTD) with ubiquitin-immunoreactive neuronal inclusions (both cytoplasmic and nuclear) of unknown nature has been linked to a chromosome 17q21 region (FTDU-17) containing MAPT (microtubule-associated protein tau). 5 key findings →

Participants: 17 Evidence: low

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

Investigating the role of rare heterozygous TREM2 variants in Alzheimer's disease and frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Neurobiology of aging 2013-10-09

Homozygous mutations in exon 2 of TREM2, a gene involved in Nasu-Hakola disease, can cause frontotemporal dementia (FTD). 4 key findings →

Design: meta-analysis Evidence: high

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

A C9orf72 promoter repeat expansion in a Flanders-Belgian cohort with disorders of the frontotemporal lobar degeneration-amyotrophic lateral sclerosis spectrum: a gene identification study

✓ Peer-reviewed alzhub usefulness score 61 out of 100. The Lancet. Neurology 2011-12-07

A locus on chromosome 9p21 has been associated with both disorders, and we aimed to identify the causal gene within this region. 3 key findings →

Participants: 305 Evidence: moderate

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

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

↑ 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