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Find studies

Showing 1–25 of 29 studies in Long-term cohort studies published 2026 (page 1 of 2) · 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.

What “Long-term cohort studies” covers

Long-term cohort studies — Large groups of people followed for years, tracking who develops dementia and what came before it.

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.

Delirium and adverse clinical outcomes: a matched cohort study in the UK Biobank

✓ Peer-reviewed alzhub usefulness score 62 out of 100. The Lancet Healthy Longevity 2026-01-01

Over a maximum follow-up of 26 years, the median time to event was 1·2 years (IQR 0·2-3·3) in the delirium group and 1·3 years (0·3-3·6) in the control group. 5 key findings →

Design: cohort study Participants: 909 Evidence: moderate

Oral health, genetic susceptibility, and risk of dementia: a prospective cohort study of UK Biobank

✓ Peer-reviewed alzhub usefulness score 57 out of 100. GeroScience 2026-05-22

Poor oral health and genetic susceptibility have each been linked to dementia risk, but their joint effects and subtype-specific associations remain unclear. 5 key findings →

Design: cohort study Participants: 7,553 Evidence: moderate

Shorter LTL was associated with an increased risk of NDDs, including Alzheimer's disease (HR: 0.52, 95% CI 0.40-0.67, P < 0.001), dementia in AD (HR: 0.53, 95% CI 0.39-0.73, P < 0.001), unspecified dementia (HR: 0.74, 95% CI 0.58-0.95, P < 0.05), degenerative diseases of the nervous system (including other specified degenerative diseases such as circumscribed brain atrophy and senile degeneration of the brain) (HR: 0.62, 95% CI 0.45-0.84, P < 0.01), extrapyramidal and movement disorders (including other specified extrapyramidal and movement disorders such as a range of tremors, chorea, tics, and other abnormal involuntary movements) (HR: 0.63, 95% CI 0.48-0.82, P < 0.01), and mental and behavioral disorders due to use of alcohol (HR: 0.46, 95% CI 0.38-0.55, P < 0.001). 5 key findings →

Participants: 459,902 Evidence: moderate

Vestibular disorders were linked to higher risks of all‐cause dementia (HR 1.86 and 95% CI 1.04–3.30), Alzheimer's disease (AD, 2.36, and 1.01–5.51), and vascular dementia (VD, 3.35, and 1.48–7.59). 5 key findings →

Design: cohort study Evidence: moderate

During a median 13.7 years of follow-up, prediabetes (n=52,693) was associated with higher risks of vascular dementia (hazard ratio (HR):1.36; 95% confidence interval (CI): 1.14-1.61), stroke (HR:1.09; 95% CI: 1.01-1.16), ischemic stroke (HR:1.10; 95% CI: 1.02-1.19), and intracerebral hemorrhage (HR:1.19; 95% CI: 1.01-1.39) compared with normoglycemia, after adjustment for major confounding factors and across extensive sensitivity analyses. 5 key findings →

Participants: 52,693 Evidence: moderate

During a median 13.7 years of follow-up, prediabetes (n=52,693) was associated with higher risks of vascular dementia (hazard ratio (HR):1.36; 95% confidence interval (CI): 1.14-1.61), stroke (HR:1.09; 95% CI: 1.01-1.16), ischemic stroke (HR:1.10; 95% CI: 1.02-1.19), and intracerebral hemorrhage (HR:1.19; 95% CI: 1.01-1.39) compared with normoglycemia, after adjustment for major confounding factors and across extensive sensitivity analyses. 5 key findings →

Participants: 52,693 Evidence: moderate

Inflammatory responses are characterized by the activation of immune cells, while inflammatory biomarkers intricately interact with the immune system. 4 key findings →

Design: cross-sectional Evidence: moderate

Three subtypes emerged: severe obesity-related inflammatory diabetes (SOID), mild metabolic diabetes (MMD, reference), and mild age-related hypertension-predominant diabetes (MARD-H). 5 key findings →

Evidence: low

Accurate dementia risk prediction is challenging, and may be facilitated by better use of imaging and genetic data, including their complex interactions. 1 key finding →

Design: post-hoc analysis Participants: 3,521 Evidence: low

Our findings reinforce the notion of a bidirectional association between epilepsy and AD, providing proof-of-concept that epilepsy, especially late-onset, may be successfully integrated into AD risk frameworks. 5 key findings →

Evidence: moderate

Impairment in the comprehension of morphosyntactic and transitivity information does not feature in current diagnostic guidelines for primary progressive aphasia (PPA) or Alzheimers Diseases (AD), despite research reporting delayed sensitivity or insensitivity of these clinical populations to these linguistic domains. 2 key findings →

Evidence: low

DNA cytosine modifications play a crucial role in gene regulation that underlies the pathogenesis of complex diseases such as Alzheimer’s disease (AD). 2 key findings →

Evidence: low

The transition to retirement and dementia risk: An application of sequence analysis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-09

Retirement timing alone showed limited association with later-life dementia risk, whereas sustained part-time employment and disability-related trajectories were more strongly associated with dementia risk. 5 key findings →

Participants: 13,879 Evidence: low

A Pipeline for ADNI Resting-State Functional MRI Processing and Quality Control

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-06

The Alzheimer’s Disease Neuroimaging Initiative (ADNI) provides a comprehensive multimodal neuroimaging resource for studying aging and Alzheimer’s disease (AD). 5 key findings →

Design: longitudinal study Evidence: moderate

Alzheimer's disease classification by means of Magnetic Resonance Imaging demands strong models that are able to generalise to different stages of dementia. 2 key findings →

Evidence: low

Proteomic signatures of APOE ε4 across human tissues and cell types in Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-03

The apolipoprotein E ε4 ( APOE ε4) allele is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD), yet its associated protein changes across biofluids, brain regions, and cell types remain incompletely understood. 3 key findings →

Participants: 1,691 Evidence: moderate

A biphasic astrocytic PTGDS trajectory marks a metabolic vulnerability stage in prodromal Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-27

PTGDS followed a biphasic astrocytic trajectory with a statistically resolved donor-level inflection (quadratic term −2.27, p = 0.006; vertex at pseudo-progression score 0.47, bootstrap 95% confidence interval 0.32 to 0.53). 5 key findings →

Design: longitudinal study 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. 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