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Find studies

Showing 501–525 of 1,328 studies of type cross-sectional study (page 21 of 54) · 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: Cross-sectional 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 Alzheimer's Disease Neuroimaging Initiative (ADNI) measures abilities broadly related to executive function (EF), including WAIS-R Digit Symbol Substitution, Digit Span Backwards, Trails A and B, Category Fluency, and Clock Drawing. 4 key findings →

Design: cross-sectional Evidence: low

In each cohort, achieving just 10-21.4 min/day moderate-to-vigorous PA related to better executive function ( P P = .02). 3 key findings →

Design: cross-sectional Participants: 1,861 Evidence: moderate

The sample included 2 619 464 patients (mean [SD] age, 81.3 [8.6] years; 61% women; 87% were White; 8% were Black; 22% with ADRD). 5 key findings →

Design: cross-sectional Participants: 464 Evidence: low

Plasma p-tau217 and p-tau231 were most effective in diagnosing aMCI/AD (AUC = 0.95 and 0.93, respectively), while p-tau217, p-tau231 and p-tau181 presented the best differential diagnosis for AD from PSP, FTD and DLB respectively (AUC = 0.84, 0.81 and 0.83). α-synuclein was presented as the best biomarker for PSP variant and behavior variant FTD subtypes (AUC = 0.81 and 0.74, respectively). 5 key findings →

Design: cross-sectional Participants: 668 Evidence: moderate

Self- and Informant-Report Cognitive Decline Discordance and Mild Cognitive Impairment Diagnosis

✓ Peer-reviewed alzhub usefulness score 56 out of 100. JAMA Network Open 2025-04-18

ADNI participants (921 dyads) had a mean (SD) age of 71 (7) years and mean (SD) of 17 (3) years of education; 485 (53%) were female, 30 (3%) were Asian, 105 (11%) were Black, and 756 (82%) were White. eVAL participants (279 dyads) had a mean (SD) age of 71 (8) years and mean (SD) of 17 (2) years of education; 151 (54%) were female, 17 (6%) were Asian, 12 (4%) were Black, and 245 (88%) were White. 5 key findings →

Design: cross-sectional Participants: 921 Evidence: moderate

Residents' QoL was negatively associated with advanced dementia, PDU, and NPS. 5 key findings →

Design: cross-sectional Participants: 207 Evidence: low

Tau PET patterns mirror clinical and neuroanatomical variability in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Brain 2016-03-08

Using PET brain scans, researchers found that where tau protein tangles build up in the brain closely tracks which brain regions lose function and matches a person's specific symptoms (memory loss vs. language problems vs. visual problems), much more closely than where amyloid plaques sit. 4 key findings →

Design: cross-sectional Participants: 35 Evidence: moderate

Generational Differences in Age-Specific Dementia Prevalence Rates

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA Network Open 2025-06-02

In this cross-sectional study examining generational differences in age-specific dementia prevalence across the US, Europe, and England, we found that individuals from more recent birth cohorts had lower proportions of people with dementia. 4 key findings →

Design: cross-sectional Participants: 62,437 Evidence: moderate

Similar to findings in adult mutation carriers, in the later preclinical and clinical stages of ADAD, mutation-carrying children were distinguished from control individuals by significantly higher plasma Aβ1-42 levels (mean [SD]: carriers, 18.8 [5.1] pg/mL and noncarriers, 13.1 [3.2] pg/mL; P Conclusions and relevance Children at genetic risk for ADAD have functional and structural brain changes and abnormal levels of plasma Aβ1-42. 2 key findings →

Design: cross-sectional Evidence: low

Association of Sleep and β-Amyloid Pathology Among Older Cognitively Unimpaired Adults

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA network open 2021-07-01

Amyloid PET and sleep duration information was acquired on 4425 cognitively unimpaired participants (mean [SD] age, 71.3 [4.7] years; 2628 [59.4%] female; 1509 [34.1%] tested Aβ positive). 4 key findings →

Design: cross-sectional Evidence: low

Regional sex-related differences in tau PET burden may contribute to the disparities in AD prevalence between males and females. 4 key findings →

Design: cross-sectional Participants: 148 Evidence: moderate

Neurodegeneration, synaptic dysfunction, and gliosis are phenotypic of Alzheimer dementia

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurology 2018-06-29

These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired. 4 key findings →

Design: cross-sectional Participants: 79 Evidence: low

These results suggest that the presence of objective memory impairment in patients with probable CAA could serve as a marker for underlying tau pathology. 4 key findings →

Design: cross-sectional Participants: 39 Evidence: low

Age-related frailty and disease-related frailty may represent different degrees of frailty severity on a biological level. 5 key findings →

Design: cross-sectional Participants: 1,199 Evidence: low

Individuals with DS were more likely to have microbleeds than controls (20% vs 8.9%, p 60 years) and AD clinical stage (12.42% asymptomatic, 27.9% prodromal, 35.09% dementia) were more common in APOE ε4 carriers (26% vs 18.3% noncarriers, p = 0.008), but not associated with vascular risk factors ( p > 0.05). 4 key findings →

Design: cross-sectional Participants: 276 Evidence: low

Infant ε4 carriers had lower MWF and GMV measurements than noncarriers in precuneus, posterior/middle cingulate, lateral temporal, and medial occipitotemporal regions, areas preferentially affected by AD, and greater MWF and GMV measurements in extensive frontal regions and measurements were also significant in the subset of 2- to 6-month-old infants (MWF differences, P Conclusions and relevance While our findings should be considered preliminary, this study demonstrates some of the earliest brain changes associated with the genetic predisposition to AD. 1 key finding →

Design: cross-sectional Evidence: low

Odor identification and Alzheimer disease biomarkers in clinically normal elderly

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurology 2015-05-01

Our objective was to investigate cross-sectional associations between odor identification ability and imaging biomarkers of neurodegeneration and amyloid deposition in clinically normal (CN) elderly individuals, specifically testing the hypothesis that there may be an interaction between amyloid deposition and neurodegeneration in predicting odor identification dysfunction. 1 key finding →

Design: cross-sectional Evidence: low

Myo-inositol changes precede amyloid pathology and relate to APOE genotype in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurology 2016-04-15

Amyloid-positive cognitively healthy participants showed a significant increase in mI/creatine and mI/NAA levels compared to amyloid-negative healthy elderly (p Conclusions mI levels are elevated already at asymptomatic stages of AD. 2 key findings →

Design: cross-sectional Evidence: low

Specific hippocampal volume reductions in individuals at risk for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurobiology of aging 1997-03-01

Our goal was to ascertain the involvement of the temporal lobe in the preclinical (not yet diagnosable) stages of dementia of the Alzheimer's type (DAT) by using MRI-derived volumes. 2 key findings →

Design: cross-sectional Participants: 22 Evidence: low

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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