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 201–225 of 2,931 studies published 2025 · free to read (page 9 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.

GLP-1RA and SGLT2i Medications for Type 2 Diabetes and Alzheimer Disease and Related Dementias

✓ Peer-reviewed alzhub usefulness score 61 out of 100. JAMA Neurology 2025-04-07

This study included 33 858 patients in the GLP-1RA vs other GLD cohort (mean age, 65 years; 53.1% female), 34 185 patients in the SGLT2i vs other GLD cohort (mean age, 65.8 years; 49.3% female), and 24 117 patients in the GLP-1RA vs SGLT2i cohort (mean age, 63.8 years; 51.7% female). 5 key findings →

Participants: 33 Evidence: moderate

Unraveling the role of proteins in dementia: insights from two UK cohorts with causal evidence

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Brain Communications 2025-01-01

NEFL (hazard ratio [HR] [95% confidence intervals (CIs)]: 1.54 [1.29, 1.84]) and RPS6KB1 (HR [95% CI]: 1.33 [1.16, 1.52]) were robustly associated with incident all-cause dementia; MMP12 (HR [95% CI]: 2.06 [1.41, 2.99]) was associated with vascular dementia in ELSA, after correcting for multiple testing. 3 key findings →

Design: longitudinal study Participants: 3,249 Evidence: moderate

Moving beyond the prevalent exposure design for causal inference in dementia research

✓ Peer-reviewed alzhub usefulness score 61 out of 100. The Lancet Healthy Longevity 2025-01-30

As randomised trials are not always feasible or practical, observational studies remain crucial for addressing many causal questions in the dementia prevention field. 1 key finding →

Design: cohort study Evidence: high

White matter hyperintensity spatial patterns: Risk factors and clinical correlates

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Alzheimer s & Dementia 2025-04-01

WMHs in the frontoparietal and anterior periventricular region were associated with blood pressure traits, WMH genetic risk score (GRS), baseline and decline in general cognitive performance, incident all-cause dementia, and ischemic stroke. 5 key findings →

Design: longitudinal study Participants: 2,878 Evidence: moderate

Recent studies suggest the existence of brain-first and body-first subtypes within the Lewy body disorder (LBD) spectrum, including Parkinson's disease. 1 key finding →

Participants: 173 Evidence: low

The LBD-present group had higher QSM values in the SNc (P = 0.008) than the LBD-absent group with no differences in SNr. 5 key findings →

Design: cohort study Participants: 13 Evidence: moderate

Four progression pathways were concluded from our analyses, cognitive stability (32.8 %), sequential MCI-only decline (34.9 %), accelerated MCI-to-dementia progression (15.8 %), and rapid direct conversion (16.5 %). 5 key findings →

Design: longitudinal study Participants: 1,136 Evidence: moderate

Females had higher rates of positive amyloid PET visual reads (63% vs. 59%, P < 0.001) and higher Centiloids (CLs; median 48.7 vs. 36.8, p < 0.001). 5 key findings →

Participants: 10,361 Evidence: moderate

Longitudinal analysis identified significant associations between the change in ether lipid species (including alkylphosphatidylcholine, alkenylphosphatidylcholine, lysoalkylphosphatidylcholine, and lysoalkenylphosphatidylcholine) and AD dementia conversion. 5 key findings →

Design: cross-sectional Participants: 1,393 Evidence: moderate

Choroid plexus free‐water correlates with glymphatic function in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Alzheimer s & Dementia 2025-05-01

At baseline, Aβ+ participants showed higher CP FWf, increased white matter hyperintensity (WMH) volume, and decreased diffusion tensor image analysis along the perivascular space (DTI-ALPS). 5 key findings →

Design: cohort study Participants: 216 Evidence: moderate

The global metabolic disorder, type 2 diabetes mellitus (T2DM), significantly increases the risk of cognitive dysfunction, including Alzheimer's disease (AD) and mild cognitive impairment (MCI). 5 key findings →

Design: meta-analysis Participants: 250,000 Evidence: high

Three survey rounds included 49 to 54 participants that agreed on VasCog-2 diagnostic criteria for preclinical, mild, and major dementia levels of vascular cognitive impairment (under the overarching term VCID). 5 key findings →

Participants: 49 Evidence: low

We included 147,986 participants (Chinese [n = 6,034], Filipino [n = 4,649], Japanese [n = 3,099], South Asian [n = 996], non-Latino White [n = 133,208]); the mean baseline age ranged from 69 to 72 years, and the percentage of female participants ranged from 40% to 63% across groups. 5 key findings →

Design: cohort study Participants: 6,034 Evidence: moderate

In this national case-control study of nursing home residents with ADRD receiving hospice care, initiation of benzodiazepine or antipsychotic use was associated with increased 180-day mortality. 5 key findings →

Design: case-control Participants: 139,103 Evidence: moderate

The majority of participants were female and were taking concomitant psychotropic medications (antidepressants and antipsychotics) at baseline. 3 key findings →

Design: phase-2-trial Participants: 75 Evidence: early

A distinct set of midlife depressive symptoms was associated with an increased risk of dementia, suggesting that these symptoms might be early markers of underlying neurodegenerative processes. 4 key findings →

Design: cohort Participants: 5,811 Evidence: moderate

EOAD, although sharing genes with LOAD, harbors unique genes and pathways that could be used to create better prediction models or target identification. 2 key findings →

Design: case-control Participants: 25,236 Evidence: moderate

Our findings suggest that poor olfaction is associated with multiple AD-related and other neurodegenerative processes. 5 key findings →

Design: cross-sectional Participants: 1,545 Evidence: moderate

Among adults with Down syndrome, the striatum consistently accumulates amyloid earlier than the cortex when measured with PiB. 2 key findings →

Design: longitudinal study Participants: 175 Evidence: moderate

The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia. 4 key findings →

Design: longitudinal study Participants: 350 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.

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