Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Find studies

Showing 601–625 of 3,166 studies of type cohort or longitudinal study (page 25 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.

The African American Dementia and Aging Project: an Oregon-based longitudinal study

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Frontiers in dementia 2024-11-18

AADAPt participants had risk factors for developing dementia in future, such as hypertension and hyperlipidemia, but also reported protective factors such as high social engagement. 2 key findings →

Design: longitudinal study Participants: 177 Evidence: moderate

Association Between Slow-Wave Sleep Loss and Incident Dementia

✓ Peer-reviewed alzhub usefulness score 67 out of 100. JAMA Neurology 2023-12-01

From the 868 Framingham Heart Study participants who returned for a second PSG, this cohort included 346 participants with a mean age of 69 years (range, 60-87 years); 179 (52%) were female. 4 key findings →

Design: cohort Participants: 346 Evidence: early

Prognostic Value of Blood-Based P-Tau217 Levels for Progression to Cognitive Impairment

✓ Peer-reviewed alzhub usefulness score 67 out of 100. JAMA 2026-09-15

In a pooled sample of multiple selected cohorts of cognitively unimpaired older adults, higher plasma p-tau217 levels were consistently associated with increased risk of clinical progression and accelerated cognitive decline. 5 key findings →

Design: cohort Participants: 2,684 Evidence: high

Of 23 558 people without pre-existing dementia, 4135 (17·6%) had an admission with delirium. 5 key findings →

Design: cohort Participants: 23,558 Evidence: moderate

Frailty, comorbidities, and other age-related diseases were associated with a higher risk of dementia but did not account for the elevated dementia risk observed after severe infections. 3 key findings →

Design: cohort Participants: 449,223 Evidence: moderate

Cerebrospinal fluid NFL concentration (median [interquartile range]) was higher in the AD dementia group (1479 [1134-1842] pg/mL), stable MCI group (no progression to AD during follow-up; 1182 [923-1687] pg/mL), and progressive MCI group (MCI with progression to AD dementia during follow-up; 1336 [1061-1693] pg/mL) compared with control participants (1047 [809-1265] pg/mL) (P Conclusions and relevance Cerebrospinal fluid NFL concentration is increased by the early clinical stage of AD and is associated with cognitive deterioration and structural brain changes over time. 2 key findings →

Design: longitudinal study Participants: 95 Evidence: moderate

Both high baseline GFAP (hazard ratio 3·6, 95% CI 2·2-5·7; p 42/40 , both GFAP (2·6, 1·4-5·0; p=0·0026) and amyloid β 42/40 (2·1, 1·2-3·6; p=0·0091) were independently associated with incident dementia whereas NfL was not (1·4, 0·8-2·5; p=0·28). 2 key findings →

Design: cohort study Participants: 300 Evidence: moderate

Most neuroinflammatory CSF biomarkers were associated with WML in individuals without dementia. 5 key findings →

Design: longitudinal study Participants: 247 Evidence: moderate

Sleep, 24-Hour Activity Rhythms, and Subsequent Amyloid-β Pathology

✓ Peer-reviewed alzhub usefulness score 67 out of 100. JAMA neurology 2024-08-01

Among community-dwelling adults included in this study, higher fragmentation of the 24-hour activity rhythms was associated with greater subsequent Aβ burden, especially in APOE4 carriers. 5 key findings →

Design: cohort study Participants: 639 Evidence: moderate

Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease. 3 key findings →

Design: cohort study Participants: 137 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

A combination of modifiable vascular risk factors in midlife is highly predictive of the likelihood of dementia decades later. 1 key finding →

Design: cohort study Participants: 2,767 Evidence: moderate

Vascular factors predict rate of progression in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 67 out of 100. Neurology 2007-11-01

Atrial fibrillation, hypertension, and angina were associated with a greater rate of decline and may represent modifiable risk factors for secondary prevention in Alzheimer disease. 3 key findings →

Design: longitudinal study Participants: 135 Evidence: moderate

Our results suggest that having an increased body weight or abdominal obesity are associated with increased dementia incidence. 5 key findings →

Design: longitudinal study Participants: 453 Evidence: moderate

Cox regression and accelerated failure time models were used to investigate whether sex, apolipoprotein E genotype and e4 carriage were associated with amyloid onset age in all cohorts. 5 key findings →

Design: longitudinal study Evidence: moderate

Insulin resistance causes diminished glucose uptake in similar regions of the brain in Alzheimer's disease (AD) and type 2 diabetes mellitus (DM2). 4 key findings →

Design: longitudinal study Participants: 26 Evidence: moderate

↑ Change the filters

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