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.
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
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
619 Colombian API registrants were prescreened, 315 were assessed for eligibility, and 252 were enrolled (crenezumab-carrier, n=85; placebo-carrier, n=84; placebo-non-carrier, n=83; 160 [63%] women and 92 [37%] men) between Dec 20, 2013, and Feb 27, 2017. 237 (94%) completed the trial, with final data collection on March 22, 2022. 5 key findings →
Participants: 85 Evidence: high
Full summary, score breakdown and related studies → Original source
Between Aug 28, 2013, and Dec 21, 2015, we enrolled 3494 participants (3061 at high risk and 433 at low risk). 5 key findings →
Design: clinical trial Participants: 3,494 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
In this meta-analysis, consistent results suggest that gantenerumab is not safe and efficient for early AD, showing no improvement in clinical scores for AD and being associated with the occurrence of ARIA-E and ARIA-H. 3 key findings →
Design: meta-analysis Participants: 2,848 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
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
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
Of 74 participants who were recruited into the OLE study between June 3, 2020, and April 22, 2021, 73 were enrolled and received gantenerumab treatment. 47 (64%) stopped dosing due to early termination of the study by the sponsor, and 13 (18%) prematurely discontinued the study for other reasons; 13 people completed 3 years of treatment. 5 key findings →
Design: clinical trial Participants: 53 Evidence: high
Full summary, score breakdown and related studies → Original source
Between July 22, 2014, and May 17, 2018, 261 participants entered the open-label phase. 211 were randomly assigned losartan (n=105) or placebo (n=106). 5 key findings →
Design: randomized controlled trial Participants: 105 Evidence: high
Full summary, score breakdown and related studies → Original source
Atypical antipsychotic drugs may be associated with a small increased risk for death compared with placebo. 2 key findings →
Design: meta-analysis Participants: 3,353 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Galantamine failed to significantly influence conversion to dementia. 3 key findings →
Participants: 2,048 Evidence: high
Full summary, score breakdown and related studies → Original source
All patients completed 100%of study visits and infusions. 5 key findings →
Participants: 18 Evidence: high
Full summary, score breakdown and related studies → Original source
From May 13, 2015, to July 22, 2020, 185 participants with Down syndrome were assessed for eligibility and 160 (86%) were randomly assigned either memantine (n=81) or placebo (n=79). 5 key findings →
Design: clinical trial Participants: 81 Evidence: high
Full summary, score breakdown and related studies → Original source
EVOKE (ClinicalTrials.gov NCT04777396) and EVOKE+ (NCT04777409) tested whether oral semaglutide, the GLP-1 diabetes/weight-loss drug, could slow early Alzheimer's disease progression in a combined 3,808 participants over up to 156 weeks. 4 key findings →
Design: phase-3-trial Participants: 3,808 Evidence: null result
Full summary, score breakdown and related studies → Original source
There were 813 participants in CREAD (mean [SD] age, 70.7 [8.2] years; 483 female and 330 male) and 806 in CREAD2 (mean [SD] age, 70.9 [7.7] years; 456 female and 350 male). 2 key findings →
Design: clinical trial Participants: 3,664 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In a large placebo-controlled randomized trial, we found that pantoprazole is not associated with any adverse event when used for 3 years, with the possible exception of an increased risk of enteric infections. 5 key findings →
Design: randomized controlled trial Participants: 8,791 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Enrollment was undertaken between May 18, 2021, and September 8, 2023. 2 key findings →
Design: clinical trial Participants: 210 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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 →