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In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Find studies

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.

A significant drug-placebo difference on the ADAS-Cog12 favoring GV-971 was present at each measurement time point, measurable at the week 4 visit and continuing throughout the trial. 3 key findings →

Design: clinical trial Participants: 818 Evidence: high

Common genetic variance in apolipoprotein E (APOE), β-glucocerebrosidase (GBA), microtubule-associated protein tau (MAPT), and α-synuclein (SNCA) has been linked to cognitive decline in Parkinson's disease (PD), although studies have yielded mixed results. 4 key findings →

Design: longitudinal study Participants: 281 Evidence: moderate

In addition, the underlying mechanism and driven mediators are largely unknown. 4 key findings →

Design: cohort study Participants: 154,549 Evidence: moderate

Identifying independent and interactive associations of a wide range of diseases and multimorbidity and apolipoprotein E4 (APOE4) with dementia may help promote cognitive health. 4 key findings →

Design: cohort study Participants: 471,485 Evidence: moderate

Future well-designed longitudinal researches examining the direct and indirect relationship between tooth loss and dementia risk are encouraged. 5 key findings →

Design: systematic review Evidence: high

Given the inconsistent evidence regarding hearing aid use and reduced dementia risk, this study evaluates whether hearing aid use, particularly effective use, is associated with lower probable dementia risk among hearing-impaired older adults. 2 key findings →

Design: cohort Participants: 61,089 Evidence: moderate

The weighted prevalence of dementia at provincial level in China in 2018 ranged from 2.62% (95%BCI: 1.70%, 3.91%) to 13.53% (95%BCI: 8.82%, 20.93%). 5 key findings →

Design: longitudinal study Participants: 17,176 Evidence: moderate

Among 331,731 participants (mean ± SD age, 56.53 ± 8.1 years; 156,762 [47.26 %] male), 4413 (1.33 %) developed dementia during a mean follow-up of 12.8 years. 5 key findings →

Design: cohort study Participants: 331,731 Evidence: moderate

Out of 462,327 eligible participants, those with constipation were associated with higher incidence of three outcome diseases (1415/20,263 [7.0%]) than those without (18,848/442,064 [4.3%]), with adjusted hazard ratio (HR) being 1.35 [1.27-1.42]. 5 key findings →

Design: cohort study Evidence: moderate

The molecular signatures of cells in the brain have been revealed in unprecedented detail, yet the ageing-associated genome-wide expression changes that may contribute to neurovascular dysfunction in neurodegenerative diseases remain elusive. 3 key findings →

Evidence: low

The differential diagnosis of frontotemporal dementia (FTD) and Alzheimer's disease (AD) is difficult due to the overlaps of clinical symptoms. 4 key findings →

Participants: 47 Evidence: low

Age is characterized by chronic inflammation, leading to synaptic dysfunction and dementia because the clearance of protein waste is reduced. 4 key findings →

Evidence: low

• Limited evidence links air pollution-lifestyle interplay to cardiovascular disease. • Study includes over 5.8 million participants from arid Northwestern China. • Air pollution in dust-prone areas is linked to cardiovascular disease. • Exercise is crucial in reducing the risk of cardiovascular disease from air pollution. • Air pollution and unhealthy lifestyles jointly heighten cardiovascular risk. 4 key findings →

Evidence: low

The 12 risk factors account for 60.3% of dementia cases in China, including 14.0% in early life, 8.8% in midlife, and 37.5% in later life. 5 key findings →

Design: longitudinal study Evidence: moderate

Elevated CKM risk level is significantly associated with increased risks of cognitive decline and dementia incidence. 3 key findings →

Participants: 426 Evidence: low

Hippocampal and serum irisin levels were progressively reduced in CCH mice. 5 key findings →

Participants: 212 Evidence: low

To the Editor: The standardized management of pain–agitation–delirium (PAD) represents a fundamental component of clinical practice in intensive care units (ICUs).[1] Evidence-based analgesia and sedation strategies not only alleviate patients’ physiological discomfort and psychological distress, but also significantly reduce mechanical ventilation duration, improve long-term prognosis, and optimize healthcare resource allocation.[1,2] Equally crucial is delirium management, as evidenced by studies demonstrating that delirium duration independently predicts mortality risk, hospital stay length, healthcare expenditures, and acquired dementia incidence.[3] Although existing studies have explored PAD management practices, most rely on clinicians’ subjective recall that may distort objective clinical realities and fail to reflect distinctive characteristics.[4] Therefore, this nationwide multicenter cross-sectional study, initiated by the Critical Care Analgesia and Sedation Quality Control Subspecialty Group under the China National Center for Medical Quality Control in Critical Care Medicine, aims to investigate the current status of PAD management in China. 5 key findings →

Design: cross-sectional Participants: 2,627 Evidence: moderate

Sodium glucose cotransporter 2 (SGLT2) inhibitors originally developed for the treatment of type 2 diabetes are clinically very effective drugs halting chronic kidney disease progression. 4 key findings →

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.

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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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