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Find studies

Showing 376–400 of 1,649 studies of type cohort or longitudinal study · free to read (page 16 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.

Mild cognitive impairment: a concept in evolution

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Journal of internal medicine 2014-03-01

The construct of mild cognitive impairment (MCI) has evolved over the past 10 years since the publication of the new MCI definition at the Key Symposium in 2003, but the core criteria have remained unchanged. 1 key finding →

Design: longitudinal study Evidence: moderate

We found that amyloid-β-positive cognitively unimpaired individuals were mainly characterized by decreased functional connectivity between the medial temporal lobe and regions in the anterior-temporal system, most prominently between left perirhinal/entorhinal cortices and medial prefrontal cortex. 5 key findings →

Design: longitudinal study Evidence: moderate

The 52 baseline participants comprised autosomal dominant Alzheimer's disease mutation carriers (n = 11; 49.6 ± 10.3 years old) and non-carriers (n = 16; 51.1 ± 14.2 years old; 10 male), and patients with sporadic mild cognitive impairment (n = 17; 61.9 ± 6.4 years old; nine male) and sporadic Alzheimer's disease (n = 8; 63.0 ± 6.5 years old; five male); for confidentiality reasons, the gender of mutation carriers is not revealed. 3 key findings →

Design: longitudinal study Evidence: moderate

GBA mutations (β = 4.65; 95% CI, 1.72-7.58; P = .002), E326K (β = 3.42; 95% CI, 0.66-6.17; P = .02), and GBA variants combined as a single group (β = 4.01; 95% CI, 1.95-6.07; P = 1.5 × 10-4) were associated with a more rapid decline in MDS-UPDRS III score. 4 key findings →

Design: longitudinal study Participants: 740 Evidence: moderate

This fifteen-year study provides a large database of highly characterized individuals with longitudinal cognitive, imaging and lifestyle data and biofluid collections, to aid in the development of interventions to delay onset, prevent or treat AD. 1 key finding →

Design: cohort study Participants: 1,112 Evidence: moderate

ADCOMS is proposed as new standard outcome for pAD and mild AD dementia trials, and is progressing in a CAMD-sponsored qualification process for use in registration trials of pAD. 3 key findings →

Design: longitudinal study Evidence: moderate

Alzheimer disease comorbid pathologic characteristics are common and are associated with more rapid cognitive decline in patients with dementia with Lewy bodies (DLB); therefore, it is anticipated that plasma p-tau concentrations may have utility in assessing cognitive impairment in individuals with this disorder. 4 key findings →

Design: cohort study Participants: 371 Evidence: moderate

The ε4 allele of apolipoprotein E (APOE) gene and increasing age are two of the most important known risk factors for developing Alzheimer disease (AD). 4 key findings →

Design: cohort study Participants: 1,593 Evidence: moderate

Cognitive decline is a debilitating manifestation of disease progression in Parkinson's disease. 4 key findings →

Design: longitudinal study Participants: 3,200 Evidence: moderate

The impact of Parkinson's disease (PD) dementia is substantial and has major functional and socioeconomic consequences. 4 key findings →

Design: longitudinal study Participants: 486 Evidence: moderate

Retinal structures may serve as a biomarker for dementia, but longitudinal studies examining this link are lacking. 4 key findings →

Design: longitudinal study Participants: 5,065 Evidence: moderate

Late-life depression (LLD) is characterized by considerable heterogeneity in clinical manifestation. 4 key findings →

Design: longitudinal study Participants: 996 Evidence: moderate

Increasing evidence suggests an association between pro-inflammatory diets and cognitive function. 4 key findings →

Design: cohort study Participants: 1,372 Evidence: moderate

Data were drawn from the UK Biobank cohort study with a total of 228 223 participants with Hospital Episodes Statistics and primary care linkage health records. 4 key findings →

Design: cohort study Participants: 2,378 Evidence: moderate

It is uncertain whether typical variants causing monogenic stroke are associated with cerebrovascular disease in the general population and why the phenotype of these variants varies so widely. 4 key findings →

Design: cohort study Participants: 454 Evidence: moderate

Longitudinal tau positron emission tomography (PET) is a relevant outcome in clinical trials evaluating disease-modifying therapies in Alzheimer disease (AD). 4 key findings →

Design: cohort study Participants: 215 Evidence: moderate

Much of late life cognitive decline is not due to common neurodegenerative pathologies

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Annals of neurology 2013-07-10

The pathologic indices of Alzheimer disease, cerebrovascular disease, and Lewy body disease accumulate in the brains of older persons with and without dementia, but the extent to which they account for late life cognitive decline remains unknown. 4 key findings →

Design: longitudinal study Participants: 856 Evidence: moderate

Both early life and adult socioeconomic status (SES) predict late-life level of memory; however, evidence is mixed on the relationship between SES and rate of memory decline. 4 key findings →

Design: longitudinal study Participants: 10,781 Evidence: moderate

One hundred eighty-seven participants with brain autopsy (NPDx1: AD n = 85; other n = 102; mean age: 74.3 years, 38.5% female; interval blood collection-death [mean ± SD]: 2.8 ± 1.6 years) and 67 NC without brain autopsy (mean age: 66.5 years, 71.6% female) were included. pTau217, but not GFAP, levels increased stepwise with increasing Thal phases (β = 0.61; 95% CI [0.24-0.97] to β = 0.91 [0.55-1.27]) and Braak stages (β = 0.59; [0.16-1.01] to β = 0.74 [0.33-1.15]). 5 key findings →

Design: cohort study Participants: 85 Evidence: moderate

Long-Term Intake of Red Meat in Relation to Dementia Risk and Cognitive Function in US Adults

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Neurology 2025-01-15

= 0.04). Replacing 1 serving per day of nuts and legumes for processed red meat was associated with a 19% lower risk of dementia (HR 0.81, 95% CI 0.75-0.86), 1.37 fewer years of cognitive aging (95% CI -2.49 to -0.25), and a 21% lower risk of SCD (RR 0.79, 95% CI 0.68-0.92). 4 key findings →

Design: cohort study Evidence: moderate

Antidepressant use and cognitive decline in patients with dementia: a national cohort study

✓ Peer-reviewed alzhub usefulness score 66 out of 100. BMC Medicine 2025-02-24

We included 18740 patients (10 205 women [54.5%]; mean [SD] age, 78.2[7.4] years), of which 4271 (22.8%) received at least one prescription for an antidepressant. 5 key findings →

Design: cohort study Participants: 18,740 Evidence: moderate

Despite remarkable progress in the biomarker field in recent years, local validation of plasma biomarkers of Alzheimer’s disease (AD) and dementia is still lacking in Latin America. 5 key findings →

Design: cohort study Participants: 49 Evidence: moderate

Higher adherence to the MedDiet was associated with greater gut microbial diversity (p < 0.05) and distinct microbial composition (PERMANOVA, p = 0.001). 5 key findings →

Design: longitudinal study Participants: 746 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