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Research

28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 26 studies in Genetics in Annals of Neurology (page 1 of 2) · 28,580 in the whole library · How the 0–100 score works

Download bibliography of these 26 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; 14,058 studies have no institution on record and are not counted here.

What “Genetics” covers

Genetics — Inherited risk: APOE and the other risk genes, and what they do and don't tell you.

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.

CR1 is associated with amyloid plaque burden and age-related cognitive decline

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Annals of neurology 2011-03-09

We found that common variation at the CR1 locus has a broad impact on cognition and that this effect is largely mediated by an individual's amyloid plaque burden. 4 key findings →

Design: cohort study Participants: 1,666 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Value of serum nonceruloplasmin copper for prediction of mild cognitive impairment conversion to Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Annals of neurology 2014-04-14

Among the evaluated parameters, the only significant predictor of conversion to AD was non-Cp copper (hazard ratio = 1.23, 95% confidence interval = 1.03-1.47, p = 0.022); for each additional micromole per liter unit (μmol/l) of non-Cp copper, the hazard increased by ~20%. 2 key findings →

Design: meta-analysis Participants: 42 Evidence: high

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

Genetic risk for Alzheimer disease is distinct from genetic risk for amyloid deposition

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Annals of Neurology 2019

This study asked whether the genes that raise Alzheimer's risk are the same genes that cause amyloid plaques to build up in the brain, and found they are not quite the same thing. 5 key findings →

Design: case-control Participants: 770 Evidence: moderate

Full summary, score breakdown and related studies → Original source

Plasma levels of apolipoprotein E and risk of dementia in the general population

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Annals of neurology 2015-01-13

Low plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of ε2/ε3/ε4 APOE genotype. 3 key findings →

Participants: 75,708 Evidence: low

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

Prioritizing Modifiable Risk Factors for Dementia Prevention across the Spectrum of Genetic Susceptibility: A Prospective Cohort Study

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Annals of Neurology 2025-10-14

Our findings highlight the importance of personalized risk assessments and the development of tailored interventions based on genetic background to prevent dementia more effectively. 5 key findings →

Design: cohort Participants: 182,473 Evidence: moderate

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

Rare coding mutations identified by sequencing of Alzheimer disease genome-wide association studies loci

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Annals of neurology 2015-07-28

Targeted sequencing of confirmed GWAS loci revealed an excess burden of deleterious coding mutations in LOAD, with the greatest burden observed in ABCA7 and BIN1. 4 key findings →

Participants: 176 Evidence: low

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

Apolipoprotein E-dependent accumulation of Alzheimer disease-related lesions begins in middle age

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Annals of neurology 2009-06-01

The brain changes associated with AD may already begin developing early in middle age, especially among APOE epsilon 4 carriers. 5 key findings →

Participants: 603 Evidence: low

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

APOEε2 is associated with milder clinical and pathological Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Annals of neurology 2015-06-01

Even when adjusted for age at onset, symptom duration, and other demographic variables, APOEε2 is associated with milder AD pathology and less severe antemortem cognitive impairment compared to APOEε3 and ε4 alleles, suggesting a relative neuroprotective effect of APOEε2 in AD. 3 key findings →

Evidence: moderate

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

Effect of apolipoprotein E on biomarkers of amyloid load and neuronal pathology in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Annals of neurology 2010-03-01

Low CSF Abeta(1-42) (surrogate for Abeta amyloid load) is more closely linked to the presence of APOE epsilon4 than to clinical status. 3 key findings →

Participants: 399 Evidence: low

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

Effect of lifestyle activities on Alzheimer disease biomarkers and cognition

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Annals of neurology 2012-11-01

None of the lifestyle variables were correlated with the biomarkers, and the path associations between lifestyle variables and biomarkers were not significant (p > 0.05). 3 key findings →

Participants: 515 Evidence: low

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

Neuronal apolipoprotein E4 increases cell death and phosphorylated tau release in alzheimer disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Annals of neurology 2019-03-27

Our results demonstrate that endogenous expression of E4 by stem-cell-derived forebrain excitatory neurons predisposes neurons to calcium dysregulation and ultimately cell death. 4 key findings →

Evidence: low

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

APOE2 Exacerbates TDP-43 Related Toxicity in the Absence of Alzheimer Pathology

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Annals of neurology 2023-01-10

We found that TDP-43 overexpression induced motor function deficits, neuronal loss, and gliosis in the motor cortex, especially in APOE2 mice, with much milder or absent effects in APOE3, APOE4, or Apoe-KO mice. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

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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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.

1,034 records (3.6% 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