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
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Slowing of cognitive and functional decline, and amyloid reduction in gantenerumab group compared to placebo group were greater in Japanese-GRADUATE than in the global-GRADUATE and JP40959. 5 key findings →
Design: clinical trial Participants: 1,965 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
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
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
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
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
1795 participants with early AD were enrolled in Clarity AD, of which 1521 were ApoE ε4 heterozygotes or non-carriers (85 %). 5 key findings →
Design: clinical trial Participants: 1,795 Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a progressive, irreversible, and fatal disease for which accumulation of amyloid beta is thought to play a key role in pathogenesis. 4 key findings →
Design: clinical trial Participants: 1,638 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles. 4 key findings →
Design: clinical trial Participants: 2,129 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Resveratrol was safe and well-tolerated. 4 key findings →
Design: clinical trial Participants: 119 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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
Among persons with early Alzheimer's disease, the use of gantenerumab led to a lower amyloid plaque burden than placebo at 116 weeks but was not associated with slower clinical decline. 2 key findings →
Design: clinical trial Participants: 980 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BAN2401-G000-201 did not meet the 12-month primary endpoint. 5 key findings →
Design: clinical trial Participants: 18 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Tarenflurbil did not slow cognitive decline or the loss of activities of daily living in patients with mild AD. 3 key findings →
Design: clinical trial Participants: 1,684 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The mean CDR-SB score at baseline was approximately 3.2 in both groups. 2 key findings →
Design: clinical trial Participants: 1,795 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In patients with early Alzheimer's disease, donanemab resulted in a better composite score for cognition and for the ability to perform activities of daily living than placebo at 76 weeks, although results for secondary outcomes were mixed. 3 key findings →
Design: clinical trial Participants: 257 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Overall, 1795 participants from Core and 1612 participants with at least one dose of lecanemab (Core + OLE) were included. 1 key finding →
Design: open-label trial Participants: 1,795 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Among 2218 AMARANTH patients, the mean (SD) age was 71.3 (7.1) years, and 1177 of 2218 (53.1%) were women. 3 key findings →
Design: clinical trial Participants: 6,871 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In participants with prodromal to mild AD in this randomized clinical trial, semorinemab did not slow clinical AD progression compared with placebo throughout the 73-week study period but did demonstrate an acceptable and well-tolerated safety profile. 3 key findings →
Design: clinical trial Participants: 422 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
No clinically important adverse events were associated with treatment. 2 key findings →
Design: clinical trial Participants: 432 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
These results show that in addition to APOE ε4 allele count, severity of Aβ neuropathology and comorbid cerebrovascular pathology may be relevant for clinicians prescribing anti-Aβ monoclonal antibodies for early AD and developing individualized safety monitoring plans. 2 key findings →
Design: clinical trial Participants: 985 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
No significant difference was seen in cognitive and functional decline between early and delayed treatment groups. 4 key findings →
Design: clinical trial Participants: 85 Evidence: high
Full summary, score breakdown and related studies → Original source
SC gantenerumab at doses of up to 1,200 mg Q4W were well tolerated in participants with mild AD dementia. 2 key findings →
Design: open-label trial Participants: 225 Evidence: low
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 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 →