Donepezil may effectively and safely improve overall functioning of DS patients with severe cognitive impairment. 2 key findings →
Evidence: high
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Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
57/100
The recently published results of the 18-month randomized controlled trial of lecanemab, reporting the efficacy of the drug in slowing the progression of early Alzheimer disease, quickly led to approval by the FDA and widespread acceptance of lecanemab treatment. 4 key findings →
Design: randomized controlled trial Evidence: high
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With the moderate sample size of the current study, treatment using sodium benzoate, a DAO inhibitor, showed promise in improving cognition, especially short-term memory, in patients with aMCI. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Major depression in older adults is common and can be effectively treated with antidepressants and electroconvulsive therapy. 2 key findings →
Evidence: low
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In the context of global ageing, the prevalence of neurodegenerative diseases and dementia, such as Alzheimer's disease (AD), is increasing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Fused in sarcoma (FUS) is an RNA-binding protein that is genetically and pathologically associated with rare and aggressive forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Study objectives To examine associations between positive airway pressure (PAP) therapy, adherence and incident diagnoses of Alzheimer's disease (AD), mild cognitive impairment (MCI), and dementia not otherwise specified (DNOS) in older adults. 5 key findings →
Participants: 1,057 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
PIM use may be higher in dementia patients and their informal caregivers compared with the general older adult population. 5 key findings →
Participants: 566 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A co-morbidity score was significantly higher in AD participants compared to controls. 3 key findings →
Participants: 187 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study suggests that estrogen replacement therapy may be useful for preventing or delaying the onset of Alzheimer disease in postmenopausal women. 4 key findings →
Design: cohort study Evidence: moderate
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Alzheimer's disease (AD) is associated with abnormal tau and amyloid-β accumulation in the brain, leading to neurofibrillary tangles, neuropil threads and extracellular amyloid-β plaques. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Many drugs that target amyloid-β (Aβ) in Alzheimer disease (AD) have failed to demonstrate clinical efficacy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study compared individuals whose clinical diagnosis of Alzheimer's disease (AD) matched or did not match neuropathologic results at autopsy on clinical and functional outcomes (cognitive impairment, functional status and neuropsychiatric symptoms). 4 key findings →
Design: longitudinal study Evidence: moderate
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Although previous research has shown that initiation of postmenopausal estrogen hormone therapy (HT) in late life increases risk of dementia, animal studies and some observational studies have suggested that midlife use of HT may be beneficial; however, this has not been rigorously investigated in large population-based studies. 4 key findings →
Participants: 1,524 Evidence: low
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Among the 1665 AIBL participants (741 [44.5%] female) and 2029 ADNI participants (925 [45.6%] female), the mean (SD) age at first evaluation was 71.8 (7.1) years and 74.5 (6.7) years, respectively. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
57/100
During an average follow-up period of 14.5 years, a total of 9520 (81.1%) participants had used NSAIDs at any given time, and 2091 participants developed dementia. 5 key findings →
Participants: 11,745 Evidence: high
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Among the participants, 377 (93.5%) reported subjective memory complaints. 5 key findings →
Design: longitudinal study Participants: 403 Evidence: moderate
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The study revealed a higher prevalence of treatment preference discussions and surrogate appointments in the two northern compared to the two southern European countries. 5 key findings →
Design: cross-sectional Participants: 4,396 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with dementia with BD had a higher prevalence of comorbidities, greater use of comedications, and greater healthcare utilization and costs than patients with dementia without BD. 5 key findings →
Participants: 103,402 Evidence: low
Full summary, score breakdown and related studies → Original source
To date, the development of disease-modifying therapies for Alzheimer's disease (AD) has largely focused on the removal of amyloid beta Aβ fragments from the CNS. 4 key findings →
Participants: 59 Evidence: moderate
Full summary, score breakdown and related studies → Original source
BACE1 is a key protease controlling the formation of amyloid β, a peptide hypothesized to play a significant role in the pathogenesis of Alzheimer's disease (AD). 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
For optimal design of anti-amyloid-β (Aβ) and anti-tau clinical trials, we need to better understand the pathophysiological cascade of Aβ- and tau-related processes. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Verubecestat is a potent BACE1 enzyme inhibitor currently being investigated in Phase III trials for the treatment of mild-to-moderate and prodromal Alzheimer's disease. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
ApoE4 levels ascertained by the e4Quant test exhibited clear genotype-dependent stratification. 2 key findings →
Participants: 160 Evidence: low
Full summary, score breakdown and related studies → Original source
In animal models, the incretin hormone GLP-1 affects Alzheimer's disease (AD). 3 key findings →
Participants: 18 Evidence: high
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,106 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- FDA Approves LEQEMBI (lecanemab-irmb) Under the Accelerated Approval Pathway for the Treatment of Alzheimer's Disease
- Drug repositioning for diabetes based on 'omics' data mining
- The Prevention of Fatal Tauopathy in a Mouse Model of Alzheimer Disease by Blocking BCL2
- Repurposing Proteostasis-Modifying Drugs to Prevent or Treat Age-Related Dementia: A Systematic Review
- Effect of choline alfoscerate in older adult patients with dementia: an observational study from the claims data of national health insurance
- Melatonin and bright-light treatment for rest-activity disruption in institutionalized patients with Alzheimer's disease
- p75 neurotrophin receptor modulation in mild to moderate Alzheimer disease: a randomized, placebo-controlled phase 2a trial
- Exploring the Molecular and Biochemical Mechanisms of Aromasin in Modulating COX-2/iNOS for Alzheimer’s Disease-Associated Synaptic Dysfunction: An In Silico Drug Repurposing Study
- Phospholipase A2 activation as a therapeutic approach for cognitive enhancement in early-stage Alzheimer disease
- Eligibility for Anti-Amyloid Therapies in Patients With Biomarker-Confirmed Atypical Alzheimer Disease Phenotypes
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →