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Find studies

Showing 2,826–2,850 of 3,166 studies of type cohort or longitudinal study (page 114 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.

This study provided a preliminary examination of indices of obstructive sleep apsnea (OSA) and sleep disruptions in adults with Down syndrome (DS), and their associations with Alzheimer's disease (AD) pathology and symptomatology. 3 key findings →

Design: longitudinal study Participants: 93 Evidence: moderate

Demonstrated utility of the mCRT warrants further investigation into comparisons between the A and B versions, free versus cued recall and changes in performance over time to better understand sensitivity for tracking memory decline over time based on age and AD clinical status. 5 key findings →

Design: longitudinal study Participants: 272 Evidence: moderate

This study aims to assess the evolution of cognitive performances over a 5-year follow-up period in community-dwelling older people with negative plasma p-tau181 levels and to determine whether frailty could discriminate between those who experience cognitive decline and those who do not, in the p-tau negative groups. 4 key findings →

Design: longitudinal study Evidence: moderate

BackgroundAmyloid-negative tau-related neurodegeneration represents a non-Alzheimer biomarker-defined profile; however, its clinical heterogeneity and prognostic relevance remain unclear within Alzheimer's disease-related frameworks. 4 key findings →

Design: cohort study Participants: 1,280 Evidence: moderate

The objective of this analysis was to develop a nonlinear disease progression model, using an expanded set of covariates that captures the longitudinal Clinical Dementia Rating Scale-Sum of Boxes (CDR-SB) scores. 4 key findings →

Design: longitudinal study Evidence: moderate

The most important predictors of having a diagnosis of ADRD by the start of care OASIS assessment were a prior discharge diagnosis of ADRD among those admitted from an inpatient setting, and frequently exhibiting symptoms of confusion. 4 key findings →

Design: cohort study Evidence: moderate

Dementia Diagnosis Underreporting and Care Engagement and Planning Among Older Adults

✓ Peer-reviewed alzhub usefulness score 47 out of 100. JAMA Network Open 2026-08-26

Among 6158 person-waves with a claims-based dementia diagnosis from 3278 PWPD (3134 [50.9%] aged 65-84 years; 4282 [69.5%] female; 1176 [19.1%] non-Hispanic Black, 617 [10.0%] Hispanic, and 4256 [69.1%] non-Hispanic White), the adjusted proportion not reporting their diagnosis was 42% (95% CI, 40%-43%) among all respondents and 67% (95% CI, 64%-69%) among self-respondents. 5 key findings →

Design: cohort study Evidence: moderate

Approximately 2% of those aged ≥60 years had dementia, lower than published estimates. 5 key findings →

Design: retrospective cohort Evidence: moderate

MAs were younger, more likely to be female, less educated, had higher ADI scores, performed worse on trails B (all p < 0.05), and had lower prevalence of APOE4 + when compared to NHWs (p < 0.0001). 5 key findings →

Design: longitudinal study Participants: 1,312 Evidence: moderate

Even after accounting for established individual‐level demographic, socioeconomic, health, and genetic risk factors for cognitive decline, greater neighborhood disadvantage is associated with an accelerated rate of annualized decline in delayed recall performance across mid to late life in a community sample. 5 key findings →

Design: longitudinal study Participants: 2,554 Evidence: moderate

The cluster analysis identified 3 distinct groups: Group 1 was low resource/high distress (n = 215); Group 2 was high resource/low distress (n = 248); and Group 3 was low resource/low distress (n = 353; Figure 1). 5 key findings →

Design: longitudinal study Participants: 215 Evidence: moderate

The Centiloid method demonstrates strong intertracer and interscanner harmonization when standardized to the 11C-Pittsburgh compound B reference, with high correlation (r2 > 0.9) across 18F-labeled tracers, including florbetapir, flutemetamol, and florbetaben. 5 key findings →

Design: longitudinal study Evidence: moderate

Higher AD-PRS was associated with faster CD in the full clinical cohort and in biomarker subset, independently of APOE genotype. 5 key findings →

Design: longitudinal study Participants: 7,233 Evidence: moderate

China accounts for 1/5 of the global population and China faces a particularly heavy dementia burden due to its rapidly ageing population. 4 key findings →

Design: cohort study Evidence: moderate

Thirty-two patients met the inclusion criteria (n=11 moderate-to-severe SVD, mean age 72 ± 10 years, 6 women; n = 21 none-to-minimal SVD, mean age 70 ± 10 years, 12 women). 3 key findings →

Design: cohort study Evidence: moderate

Financial difficulties and well-being among caregivers of persons with severe dementia

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Aging & Mental Health 2025-03-25

= 0.01). We also found that greater use of emotion-focused coping and deriving greater gains in caregiving mitigated the negative association between caregiver financial difficulty and their distress and perception of PwSDs' well-being. 2 key findings →

Design: cohort study Evidence: moderate

Novel insights into Alzheimer's disease through the study of individuals with Down syndrome

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Alzheimer s & Dementia 2026-01-01

Novel insights into Alzheimer's disease through the study of individuals with Down syndromePeople with Down syndrome (DS) represent the largest genetically defined population at risk for Alzheimer's disease (AD). 1 Virtually all adults with DS develop AD neuropathology by midlife due to triplication of the amyloid precursor protein (APP) gene on chromosome 21.As medical advances and social integration have extended life expectancy into the 60s, AD has emerged as the major determinant of cognitive decline, morbidity, and mortality in this DS population. 2 What was once viewed as an inevitable consequence of aging in DS is now recognized as a unique scientific opportunity to uncover the earliest events that drive AD.The predictable and accelerated course of DS-associated AD (DSAD) provides an unparalleled window into the molecular and cellular origins of amyloid and tau pathology, neuroinflammation, cerebrovascular pathology, and neurodegeneration. 1 key finding →

Design: longitudinal study Evidence: moderate

These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer’s disease. 5 key findings →

Design: longitudinal study Participants: 132 Evidence: moderate

SSRI treatment showed no significant effect on AD dementia progression (hazard ratio = 1.64, 95% confidence interval: 0.61 to 4.38) or cognitive trajectories, regardless of AD pathology. 5 key findings →

Design: longitudinal study Evidence: moderate

Subjective cognitive decline (SCD) is increasingly recognised as a potential preclinical stage of Alzheimer's disease, yet the physiological mechanisms underlying its progression remain poorly understood. 4 key findings →

Design: longitudinal study Evidence: moderate

Dementia syndromes involve cognitive but also early motor impairment. 3 key findings →

Design: longitudinal study Participants: 104 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