These findings support further investigation of ABvac40 as a potential disease-modifying therapy. 3 key findings →
Design: clinical trial Participants: 124 Evidence: high
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
89/100
The systematic review and NMA includes 493 168 participants from 869 trials (adding 53 trials since October 2022) reporting data for 13 drug classes (63 drugs) and 26 outcomes of interest. 5 key findings →
Design: systematic review Participants: 168 Evidence: high
Full summary, score breakdown and related studies → Original source
Donanemab treatment resulted in earlier and greater AP clearance compared to aducanumab. 5 key findings →
Design: clinical trial Participants: 148 Evidence: high
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease, the spread of aberrantly phosphorylated tau is an important criterion in the Braak staging of disease severity and correlates with disease symptomatology. 4 key findings →
Participants: 654 Evidence: high
Full summary, score breakdown and related studies → Original source
Our analysis encompassed 22 RCTs involving 138,282 participants (mean age 64.8 years, 36.4% female). 5 key findings →
Design: meta-analysis Participants: 138,282 Evidence: high
Full summary, score breakdown and related studies → Original source
Seventeen studies (5373 patients) were included. 5 key findings →
Design: meta-analysis Participants: 5,373 Evidence: high
Full summary, score breakdown and related studies → Original source
Anti-amyloid-ß mAbs attenuate cognitive and functional decline compared with placebo in early AD; whether the magnitude of this effect is clinically important remains uncertain, especially relative to the safety profile of these medications. 5 key findings →
Participants: 15,275 Evidence: high
Full summary, score breakdown and related studies → Original source
Bapineuzumab did not improve clinical outcomes in patients with Alzheimer's disease, despite treatment differences in biomarkers observed in APOE ε4 carriers. 1 key finding →
Design: clinical trial Participants: 1,090 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Blarcamesine, demonstrating a safety profile with no associated neuroimaging adverse events, significantly slowed clinical progression by 36.3% at 48 weeks with blarcamesine group as well as the individual 30 mg (by 34.6%) and 50 mg (by 38.5%) blarcamesine groups vs. placebo on the prespecified primary cognitive endpoint ADAS-Cog13. 5 key findings →
Design: open-label trial Participants: 338 Evidence: high
Full summary, score breakdown and related studies → Original source
In this meta-analysis of phase III trials in AD, we found that monoclonal antibodies against Aβ induced clinical improvements of small effect sizes, biomarker improvements of large effect sizes, and increases in risk for the hallmark adverse event, ARIA, by a large effect size, when all drugs were pooled together. 4 key findings →
Design: meta-analysis Participants: 12,585 Evidence: high
Full summary, score breakdown and related studies → Original source
Despite immunotherapies significantly increasing the risks of adverse events and ARIA, the data suggest that mAbs can effectively improve the cognitive function of patients with mild and moderate AD. 5 key findings →
Design: meta-analysis Participants: 21,087 Evidence: high
Full summary, score breakdown and related studies → Original source
Efficacy, safety, biomarker, and PK profiles of aducanumab were consistent between the Japanese subgroup and the overall population. 5 key findings →
Design: clinical trial Participants: 121 Evidence: high
Full summary, score breakdown and related studies → Original source
84/100
Overall, the study drug was well tolerated. 5 key findings →
Participants: 20 Evidence: high
Full summary, score breakdown and related studies → Original source
84/100
Targeting of tau pathology has long been proposed as a potential therapeutic strategy for Alzheimer's disease (AD). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Thirty-three randomized controlled trials were identified evaluating 15,971 participants (9,103 (57%) female). 5 key findings →
Participants: 15,971 Evidence: high
Full summary, score breakdown and related studies → Original source
ARIA is an adverse event associated with donanemab treatment that requires safety monitoring. 4 key findings →
Design: phase-3-trial Participants: 3,030 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Of 3285 included participants, the mean (SD) age was 70.4 (7.45) years; 1706 participants (52%) were female, 2661 (81%) had mild cognitive impairment due to Alzheimer disease, and 1777 (54%) used symptomatic medications for Alzheimer disease. 2 key findings →
Design: clinical trial Participants: 1,087 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Selection criteria All unconfounded, double-blind, randomized controlled trials in which treatment with donepezil was compared with placebo for patients with mild, moderate or severe dementia due to Alzheimer's disease. 5 key findings →
Participants: 5,272 Evidence: high
Full summary, score breakdown and related studies → Original source
As the first NMA comparing different interventions for AD and MCI, our study suggests that PE and CCT might have a significant improvement in cognition and neuropsychiatric symptoms respectively. 4 key findings →
Design: meta-analysis Participants: 1,747 Evidence: high
Full summary, score breakdown and related studies → Original source
Amyloid-β (Aβ) plaques and aggregated tau are two core mechanisms that contribute to the clinical deterioration of Alzheimer’s disease (AD). 2 key findings →
Design: systematic review Participants: 396 Evidence: high
Full summary, score breakdown and related studies → Original source
The safety profile of aducanumab remained unchanged in the LTE of PRIME. 4 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Subgroup analyses included (i) MCI versus mild AD; (ii) with versus without concomitant AD medications; and (iii) Apolipoprotein E (ApoE4) carriers versus non-carriers. 5 key findings →
Design: randomized controlled trial Participants: 8,010 Evidence: high
Full summary, score breakdown and related studies → Original source
In a large international cardiovascular outcome trial in people with type 2 diabetes and cardiorenal disease, linagliptin did not modulate cognitive decline over 2.5 years. 2 key findings →
Participants: 1,545 Evidence: high
Full summary, score breakdown and related studies → Original source
GLP-1 RA therapy did not alter amyloid-β and tau biomarkers nor show improvements in cognition but showed potential metabolic and neuroprotective benefits. 1 key finding →
Design: systematic review Participants: 1,444 Evidence: high
Full summary, score breakdown and related studies → Original source
Memantine monotherapy improved cognition, behavior, activities of daily living, global function, and stage of dementia and was well-tolerated by AD patients. 5 key findings →
Design: meta-analysis Participants: 2,433 Evidence: high
Full summary, score breakdown and related studies → Original source
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →