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Find studies

Showing 1–25 of 110 studies in Genetics of type cohort or longitudinal study · free to read (page 1 of 5) · 28,980 in the whole library · How the 0–100 score works

Download bibliography of these 110 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.

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.

Association Between Midlife Vascular Risk Factors and Estimated Brain Amyloid Deposition

✓ Peer-reviewed alzhub usefulness score 75 out of 100. JAMA 2017-04-01

An increasing number of midlife vascular risk factors was significantly associated with elevated amyloid SUVR; this association was not significant for late-life risk factors. 5 key findings →

Design: cohort study Participants: 20 Evidence: moderate

APOE3 Christchurch Heterozygosity and Autosomal Dominant Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 72 out of 100. New England Journal of Medicine 2024-06-20

Clinical data supported a delayed onset of cognitive impairment in persons who were heterozygous for the APOE3 Ch variant in a kindred with a high prevalence of autosomal dominant Alzheimer's disease. 3 key findings →

Design: cohort Participants: 1,077 Evidence: moderate

Sex-Specific Association of Apolipoprotein E With Cerebrospinal Fluid Levels of Tau

✓ Peer-reviewed alzhub usefulness score 71 out of 100. JAMA neurology 2018-08-01

After correcting for multiple comparisons using the Bonferroni procedure, we observed a statistically significant interaction between APOE-ε4 and sex on CSF total tau (β = 0.41; 95% CI, 0.27-0.55; P Conclusions and relevance We provide robust evidence of a stronger association between APOE-ε4 and CSF tau levels among women compared with men across multiple independent data sets. 5 key findings →

Design: cohort study Participants: 1,798 Evidence: moderate

The APOE-epsilon4 allele and the risk of Alzheimer disease among African Americans, whites, and Hispanics

✓ Peer-reviewed alzhub usefulness score 70 out of 100. JAMA 1998-03-01

The presence of an APOE-epsilon4 allele is a determinant of AD risk in whites, but African Americans and Hispanics have an increased frequency of AD regardless of their APOE genotype. 2 key findings →

Design: longitudinal study Participants: 1,079 Evidence: moderate

Over 10 years of close clinical dementia surveillance in this cohort study, loneliness was associated with increased dementia risk; this tripled in adults whose baseline risk would otherwise be relatively low on the basis of age and genetic risk, representing a majority of the US population. 5 key findings →

Design: cohort study Participants: 2,308 Evidence: moderate

White Matter Abnormalities and Cognition in Aging and Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 70 out of 100. JAMA Neurology 2025-06-09

Of 4467 participants who underwent 9208 longitudinal cognitive sessions, 2698 (60.4%) were female, and the mean age (SD) was 74.3 (9.2) years; 3213 were cognitively unimpaired, 972 had mild cognitive impairment, and 282 had AD dementia. 2 key findings →

Design: cohort study Participants: 4,467 Evidence: moderate

Among the 1430 cognitively normal participants included, the mean (SD) age was 79.5 (5.3) years, 49.4% were men, the mean duration of education was 14.3 years, and 25.4% were APOE ε4 carriers. 5 key findings →

Design: longitudinal study Participants: 1,630 Evidence: moderate

Association of Cardiovascular Risk Trajectory With Cognitive Decline and Incident Dementia

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Neurology 2022-04-20

The findings of the current study show that the longitudinal, cumulative trajectory of cardiovascular risk is predictive of dementia risk and associated with the emergence of memory decline. 4 key findings →

Design: prospective cohort Participants: 1,244 Evidence: moderate

NSAID use and dementia risk in the Cardiovascular Health Study: role of APOE and NSAID type

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Neurology 2007-11-14

Use of NSAIDs was associated with a lower risk of dementia (adjusted hazard ratio or aHR 0.76, 95% CI or CI 0.60-0.96) and, in particular, AD (aHR 0.63, CI 0.45-0.88), but not VaD (aHR 0.92, CI 0.65-1.28). 3 key findings →

Design: cohort study Participants: 3,229 Evidence: moderate

Serum triglycerides in Alzheimer disease: Relation to neuroimaging and CSF biomarkers

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Neurology 2020-05-01

This study shows that PUTG component scores were significantly associated with diagnostic group and AD biomarkers, a finding that was more pronounced in APOE ε4 carriers. 5 key findings →

Design: longitudinal study Participants: 689 Evidence: moderate

These results from the largest longitudinal cohort registry of patients with CAA-ri support the transient and potentially relapsing inflammatory nature of the clinical-radiologic acute manifestations of the disease and the effectiveness of slow oral tapering off after IV corticosteroid pulse therapy in preventing recurrences. 3 key findings →

Design: longitudinal study Participants: 113 Evidence: moderate

Injury markers predict time to dementia in subjects with MCI and amyloid pathology

✓ Peer-reviewed alzhub usefulness score 67 out of 100. Neurology 2012-09-26

In subjects with MCI and evidence of amyloid pathology, the injury markers CSF t-tau and p-tau and hippocampal atrophy can predict further cognitive decline. 1 key finding →

Design: cohort study Participants: 110 Evidence: moderate

Fasting lipid fractions (triglycerides [TGs], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], total cholesterol [TC]) were studied as continuous variables, and results are reported per SD increase of each lipid fraction. 5 key findings →

Design: cohort study Participants: 9,294 Evidence: moderate

Our findings suggest that statins might be associated with a lower risk of incident AD among individuals with the APOE ε4 allele. 5 key findings →

Design: cohort Participants: 4,807 Evidence: early

New PRSs for dementia significantly improve risk-prediction performance, but still account for less risk than APOE genotype overall. 3 key findings →

Design: cohort Participants: 12,031 Evidence: moderate

Longitudinal Cerebrospinal Fluid Biomarker Changes in Preclinical Alzheimer Disease During Middle Age

✓ Peer-reviewed alzhub usefulness score 66 out of 100. JAMA neurology 2015-09-01

Within-person changes in CSF biomarkers were also compared with changes in cortical PiB binding and progression to a CDR higher than 0 at follow-up. 2 key findings →

Design: cohort study Participants: 169 Evidence: moderate

Prevalence and Clinical Phenotype of Quadruple Misfolded Proteins in Older Adults

✓ Peer-reviewed alzhub usefulness score 66 out of 100. JAMA neurology 2020-10-01

However, the clinical presentation, associated factors, frequency in community-based cohorts, genetic characteristics, and cognitive trajectories associated with the quadruple misfolded proteins phenotype are not well understood. 5 key findings →

Design: cohort study Participants: 375 Evidence: moderate

At 48 months, group differences between clinical progressors and non-progressors were significant for self (2.13, SE=0.45, P Conclusions and relevance Demonstrating long-term clinical benefit will be critical for the success of recently launched secondary prevention trials. 1 key finding →

Design: longitudinal study Participants: 468 Evidence: moderate

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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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.

1,038 records (3.6% of the library) are not peer-reviewed — 966 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