91/100
55-80 years of age were screened (N = 63,124). 5 key findings →
Design: longitudinal study Participants: 63,124 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.
Compared with placebo, treatment with mAbs significantly improved cognitive performance on CDR-SB (mean difference -0.25, 95% confidence interval [CI] [-0.38, -0.11]) and ADAS-Cog (standardized mean difference -0.09, 95% CI [-0.12, -0.06]), in which a negative change indicates improvement for both scores. 2 key findings →
Design: meta-analysis Participants: 18,826 Evidence: high
Full summary, score breakdown and related studies → Original source
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
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
Six trials (3103 Gantenerumab significantly reduces amyloid and statistically improves select functional (FAQ) and cognitive (ADAS-Cog13) measures in early AD; however, these changes remain below accepted MCID thresholds, indicating a lack of true clinical meaningfulness. 2 key findings →
Design: systematic review Participants: 3,103 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
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
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
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
Dominantly inherited Alzheimer's disease (DIAD) causes predictable biological changes decades before the onset of clinical symptoms, enabling testing of interventions in the asymptomatic and symptomatic stages to delay or slow disease progression. 2 key findings →
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
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
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
Nineteen randomized placebo-controlled trials with 6918 participants were included. rTMS was significantly more effective than placebo/sham stimulation. 5 key findings →
Design: meta-analysis Participants: 6,918 Evidence: high
Full summary, score breakdown and related studies → Original source
Lecanemab treatment resulted in significant reduction in amyloid plaques and a slowing of clinical decline. 5 key findings →
Design: open-label trial Participants: 856 Evidence: high
Full summary, score breakdown and related studies → Original source
FDA-approved anti-Aβ mabs have a role in slowing disease progression in patients with AD, at the cost of an increased probability of side effects. 3 key findings →
Design: systematic review Participants: 4,471 Evidence: high
Full summary, score breakdown and related studies → Original source
Immunotherapeutics targeting amyloid-β (Aβ) have had mixed results in clinical trials. 3 key findings →
Participants: 5,554 Evidence: high
Full summary, score breakdown and related studies → Original source
The efficacy and safety of anti-amyloid mAbs in AD may differ based on patients' demographic and genetic factors. 4 key findings →
Design: systematic review Participants: 5,633 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 →