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Find studies

Showing 1,826–1,850 of 3,166 studies of type cohort or longitudinal study (page 74 of 127) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

This list as a page: Cohort or longitudinal study in the library →

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

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.

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

Among 298 participants (MCI, n = 56; NC, n = 242; mean age 75.1 years; 45.6% female), the groups were similar in age, sex, race, and APOE ε4 status at baseline, as well as in most driving behaviors. 4 key findings →

Design: cohort Participants: 298 Evidence: early

In the intention-to-treat analysis, dementia risk was not different between GLP1-RA and DPP4i initiators (hazard ratio [HR] 0.95, 95% confidence interval [CI] 0.87–1.04; rates: 6.29 versus 6.64 per 1000 person-years; mean follow-up: 6.54 years); however, continuous GLP1-RA versus DPP4i use was associated with a 21% lower risk (HR 0.79, 95% CI 0.64–0.97; rates: 3.64 versus 4.82; mean follow-up: 2.71 years). 4 key findings →

Design: cohort Participants: 107,424 Evidence: moderate

Plasma GFAP is a prognostic biomarker in CU older adults, predicting cognitive and biological changes, with stronger associations observed in females, highlighting a possible sex-specific vulnerability. 5 key findings →

Design: cohort Participants: 949 Evidence: moderate

In DIAD, clinical disease stage and BDNF Met66 were associated with cognitive impairment and levels of site-specific tau phosphorylation. 5 key findings →

Design: cohort study Participants: 527 Evidence: moderate

These findings suggest that DPP-4i use is associated with low amyloid burden and favorable long-term cognitive outcome in diabetic patients with ADCI. 2 key findings →

Design: longitudinal study Participants: 70 Evidence: moderate

Accounting for educationalfactors, vascular factors, and Aβ burden diminished, but did not eliminate, racial differences in PACC5 performance longitudinally. 4 key findings →

Design: longitudinal study Participants: 296 Evidence: moderate

Longitudinal racial differences in amyloid biomarkers are observed. 1 key finding →

Design: longitudinal study Participants: 179 Evidence: moderate

Donepezil treatment slows the progression of hippocampal atrophy, suggesting a neuroprotective effect of donepezil in Alzheimer's disease. 2 key findings →

Design: cohort study Participants: 54 Evidence: moderate

The presence of epsilon 4 was associated with risk of developing AD on follow-up (relative risk, 1.92; 95% confidence interval, 1.27-2.89). 3 key findings →

Design: cohort study Participants: 624 Evidence: moderate

Hypothetical Preclinical Alzheimer Disease Groups and Longitudinal Cognitive Change

✓ Peer-reviewed alzhub usefulness score 58 out of 100. JAMA neurology 2016-06-01

These results suggest that, to optimize observing a treatment effect, clinical trials enrolling cognitively normal individuals should selectively recruit participants with abnormal levels of both amyloid and tau (ie, stage 2) because this group would be expected to show the greatest cognitive decline over time if untreated. 3 key findings →

Design: cohort study Evidence: moderate

Although most falls do not result in injury, the fact that residents with dementia fall more often than their counterparts without dementia leaves them with a higher overall risk of sustaining injurious falls over time. 2 key findings →

Design: cohort study Evidence: moderate

Recent findings Both of these leisure-time activities were associated with significant reductions in the risk of dementia in longitudinal studies. 4 key findings →

Design: longitudinal study Evidence: moderate

Self-reported sleep problems may increase the risk for dementia, and depressive symptoms may explain this relationship. 3 key findings →

Design: longitudinal study Evidence: moderate

Food combination and Alzheimer disease risk: a protective diet

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Archives of neurology 2010-04-12

Simultaneous consideration of previous knowledge regarding potentially AD-related nutrients and multiple food groups can aid in identifying food combinations that are associated with AD risk. 3 key findings →

Design: cohort study Evidence: moderate

The DRS-R-98, a 16-item clinician-rated scale with 13 severity items and 3 diagnostic items, was validated against the Cognitive Test for Delirium (CTD), Clinical Global Impression scale (CGI), and Delirium Rating Scale (DRS) among five diagnostic groups (N=68): delirium, dementia, depression, schizophrenia, and other. 1 key finding →

Design: longitudinal study Participants: 68 Evidence: moderate

Recent findings suggest that a rich social network may decrease the risk of developing dementia. 3 key findings →

Design: longitudinal study Evidence: moderate

19F and 1H MRI detection of amyloid beta plaques in vivo

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature neuroscience 2005-03-13

Formation of senile plaques composed of amyloid beta peptide, a pathological hallmark of Alzheimer disease, in human brains precedes disease onset by many years. 2 key findings →

Design: longitudinal study Evidence: moderate

In our study, TSH was related neither to risk of AD nor with early MRI markers thereof, arguing against an important role of thyroid function in the development of AD. 4 key findings →

Design: cohort study Participants: 1,025 Evidence: moderate

We examined longitudinal associations between the apolipoprotein E ε4 allele (ApoE4(+) status) and several cognitive outcomes and tested effect modification by sex. 3 key findings →

Design: longitudinal study Participants: 113 Evidence: moderate

These findings suggest that depressive symptoms precede memory decline, but not vice versa, in late life. 3 key findings →

Design: longitudinal study Participants: 2,425 Evidence: moderate

In these older adults, associations of risk factors with a given cause of death were related to specific deficits in that same organ system. 2 key findings →

Design: cohort study Participants: 5,888 Evidence: moderate

Estrogen deficiency and risk of Alzheimer's disease in women

✓ Peer-reviewed alzhub usefulness score 58 out of 100. American journal of epidemiology 1994-08-01

The authors explored the possibility that estrogen loss associated with menopause may contribute to the development of Alzheimer's disease by using a case-control study nested within a prospective cohort study. 4 key findings →

Design: cohort 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.

1,034 records (3.7% 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