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Find studies

Showing 601–625 of 1,649 studies of type cohort or longitudinal study · free to read (page 25 of 66) · 30,980 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)

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.

Among 2946 participants (mean [SD] age, 74.9 [4.6] years; 1751 [59.4] female; 637 Black [21.6%] and 2309 White [78.4%] individuals), 1947 participants (66.1%) had audiometric hearing loss, and 1097 (37.2%) had self-reported hearing loss. 5 key findings →

Design: cohort study Participants: 2,946 Evidence: moderate

The study sample included 1,375 participants free of dementia and stroke at baseline (mean age 68 ± 6y, 54 % females). 5 key findings →

Design: cohort study Participants: 1,375 Evidence: moderate

Distinct associations between different traffic noise exposures and incident dementia subtypes were found in this large UK prospective cohort study. 3 key findings →

Design: cohort study Participants: 502,416 Evidence: moderate

Comorbid cardiovascular and metabolic risk factors (CVM) differentially impact brain structure and increase dementia risk, but their specific magnetic resonance imaging signatures (MRI) remain poorly characterized. 1 key finding →

Design: cohort study Participants: 37,096 Evidence: moderate

A total of 60 860 adults with type 2 diabetes and obesity were included, with 30 430 each in the GLP-1RA group (mean [SD] age, 57.9 [9.9] years; 50.2% female) and the other antidiabetic drug group (mean [SD] age, 58.0 [10.8] years; 51.4% female) after propensity score matching. 5 key findings →

Design: cohort study Participants: 860 Evidence: moderate

Sex differences in the clinical manifestation of autosomal dominant frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Alzheimer s & Dementia 2025-04-01

While sex differences were not apparent at asymptomatic stages, females showed more rapid declines across all outcomes in symptomatic stages compared to males. 5 key findings →

Design: longitudinal study Participants: 337 Evidence: moderate

DOPA Decarboxylase (DDC) has been proposed as a cerebrospinal fluid (CSF) biomarker with increased concentrations in Lewy body disorders (LBDs) and highest levels in patients receiving dopaminergic treatment. 2 key findings →

Design: longitudinal study Participants: 71 Evidence: moderate

Disease-modifying effects of TMEM106B in genetic frontotemporal dementia: a longitudinal GENFI study

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Brain 2025-04-22

Common variants within TMEM106B are associated with risk for frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP). 4 key findings →

Design: cohort study Participants: 518 Evidence: moderate

Repeated plasma p‐tau217 measurements to monitor clinical progression heterogeneity

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Alzheimer s & Dementia 2025-05-01

Three progression clusters emerged in both cohorts: stable cognition, slow decline, and rapid decline-each including cases initially classified as CN or MCI. 5 key findings →

Design: longitudinal study Participants: 186 Evidence: moderate

Alzheimer's disease is a progressive neurodegenerative disorder with no cure, making preventive strategies crucial. 5 key findings →

Design: cohort study Participants: 1,500 Evidence: moderate

In those aged 65 years or older, delirium was overall associated (all p<0·001, age and sex adjusted) with dementia ( adj OR 3·63 [95% CI 2·65–4·98]), pre-admission dependency (2·63 [2·02–3·43]), comorbidity burden (1·04 [1·02–1·05]), and frailty (moderate vs low risk 3·62 [2·70–4·85] and high vs low risk 11·85 [7·24–19·42]), with stronger associations in patients without comorbid dementia than in those with comorbid dementia. 4 key findings →

Design: longitudinal study Participants: 290 Evidence: moderate

In this study, clinically normal adults with SNAP did not exhibit evidence of elevated tau levels, which suggests that this biomarker construct does not represent amyloid-independent tauopathy. 5 key findings →

Design: longitudinal study Participants: 247 Evidence: moderate

Plasma biomarkers for prognosis of cognitive decline in patients with mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Brain communications 2022-06-14

Although recent studies have demonstrated the prognostic utility of plasma biomarkers of Alzheimer pathology or neurodegeneration, such as pTau-181 and NF-L, whether other plasma biomarkers can further improve prediction of cognitive decline is undetermined. 5 key findings →

Design: cohort study Participants: 60 Evidence: moderate

Cerebral Amyloid Angiopathy and Downstream Alzheimer Disease Plasma Biomarkers

✓ Peer-reviewed alzhub usefulness score 62 out of 100. JAMA network open 2025-05-01

Lobar CMB counts and the presence of CAA were associated with downstream AD plasma biomarkers, including p-tau217 (β = 0.12 [95% CI, 0.05-0.18] and 0.29 [95% CI, 0.12-0.47], respectively), GFAP (β = 0.07 [95% CI, 0.03-0.12] and 0.20 [95% CI, 0.09-0.31], respectively), and NfL (β = 0.07 [95% CI, 0.03-0.11] and 0.16 [95% CI, 0.06-0.25], respectively) with and without the mediation of Aβ uptake on PET (indirect effect: lobar CMBs-p-tau217, 59.8% [β = 0.07 (95% CI, 0.03-0.11)]; lobar CMBs-GFAP, 49.3% [β = 0.04 (95% CI, 0.01-0.06)]; lobar CMBs-NfL, 20.9% [β = 0.01 (95% CI, 0.01-0.03)]; CAA-p-tau217, 50.9% [β = 0.15 (95% CI, 0.06-0.24)]; CAA-GFAP, 39.2% [β = 0.08 (95% CI, 0.03-0.13)]; CAA-NfL, 19.2% [β = 0.03 (95% CI, 0.01-0.05)]). 4 key findings →

Design: cohort study Participants: 1,708 Evidence: moderate

Cholesterol, APOE genotype, and Alzheimer disease: an epidemiologic study of Nigerian Yoruba

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Neurology 2006-01-01

There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans. 4 key findings →

Design: longitudinal study Participants: 1,075 Evidence: moderate

Cognitively normal elderly individuals who engage in specific mentally stimulating activities even in late life have a decreased risk of incident MCI. 3 key findings →

Design: cohort study Participants: 973 Evidence: moderate

Persons with severe CAA compared with those without CAA were more likely to carry an APOE ε4 allele (64.9% vs 42.8%, respectively; P Conclusions and relevance Being Hispanic and having had a transient ischemic attack-like episode were predictors of CAA in persons with AD. 1 key finding →

Design: longitudinal study Participants: 193 Evidence: moderate

Higher baseline PP was significantly associated with increased Aβ (β = 0.078; p = 0.001), inferior temporal tau (β = 0.110; p = 0.032), and meta-temporal tau deposition (β = 0.116; p = 0.022). 4 key findings →

Design: cohort study Participants: 1,690 Evidence: high

Risk factors for non-motor symptoms in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 62 out of 100. The Lancet. Neurology 2018-04-23

Non-motor symptoms (NMS) of Parkinson's disease can be predominant as the disease advances, thereby constituting a major source of disease burden for patients and caregivers. 2 key findings →

Design: longitudinal study Evidence: moderate

In the 852 subjects without dementia, depressed mood was more common in individuals with greater cognitive impairment. 3 key findings →

Design: longitudinal study Participants: 1,070 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.

1,042 records (3.4% of the library) are not peer-reviewed — 967 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    Where this research is being discussed: events