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Find studies

Showing 151–175 of 2,931 studies published 2025 · free to read (page 7 of 118) · 30,580 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.

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

Neurodegenerative diseases (NDs), such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and frontotemporal dementia (FTD), exhibit distinct yet overlapping pathological mechanisms. 2 key findings →

Participants: 10,527 Evidence: low

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

We aimed to conduct a cost-utility analysis of DREAMS START compared with treatment as usual (TAU). 4 key findings →

Design: RCT Participants: 377 Evidence: moderate

This meta-analysis highlights sleep management as a pivotal modifiable factor in reducing the risk of all-cause cognitive decline. 5 key findings →

Design: meta-analysis Evidence: moderate

Plasma p-tau217 and p-tau217/Aβ42 concentrations demonstrated robust diagnostic performance in a heterogeneous clinical cohort; interpretation requires consideration of kidney function. 5 key findings →

Design: cross-sectional Participants: 509 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

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

In preclinical studies, it has demonstrated vascular protective and antioxidant effects, with emerging evidence suggesting potential neuroprotective properties. 2 key findings →

Design: randomized controlled trial Participants: 185 Evidence: high

Higher plasma carotenoid concentrations were associated with slower cognitive decline in APOE ε4 carriers, potentially mitigating genetic risk. 3 key findings →

Design: randomized controlled trial Participants: 442 Evidence: high

Dementia-related blood biomarkers are the future of large-scale dementia risk stratification; however, the extent to which phosphorylated tau (P-tau181), neurofilament light (NfL), and glial fibrillary acidic protein (GFAP) are associated with nonmodifiable risk factors has yet to be confirmed in the community, and the role of menopause has yet to be investigated. 4 key findings →

Design: cohort study Participants: 9,940 Evidence: moderate

Despite the increasing approval of antiamyloid antibodies for Alzheimer disease (AD), their clinical relevance and risk-benefit profile remain uncertain. 4 key findings →

Design: meta-analysis Participants: 21,236 Evidence: high

Race and Ethnicity, Lifestyle, Diet, and Survival in Patients With Prostate Cancer

✓ Peer-reviewed alzhub usefulness score 62 out of 100. JAMA Network Open 2025-02-26

A total of 2603 men with nonmetastatic PCa (mean [SD] age, 69.6 [7.1] years) were followed up, and 1346 deaths were documented, including 356 (24.6%) from CVD and 197 (14.6%) from PCa. 5 key findings →

Design: cohort study Participants: 2,603 Evidence: moderate

Impact of Vegan and Vegetarian Diets on Neurological Health: A Critical Review

✓ Peer-reviewed alzhub usefulness score 62 out of 100. Nutrients 2025-02-28

Evidence suggests that vegan and vegetarian diets, when well planned, can be rich in phytonutrients and antioxidants, which have been associated with lower levels of inflammatory markers, such as C-reactive protein (CRP) and interleukin-6 (IL-6). 5 key findings →

Design: systematic review Evidence: high

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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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.

1,037 records (3.4% of the library) are not peer-reviewed — 964 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