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
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Forty-four participants were recruited between September 2019 and June 2022. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Risk for late-onset Alzheimer's disease (LOAD), the most prevalent dementia, is partially driven by genetics. 5 key findings →
Design: meta-analysis Participants: 94,437 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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
83/100
Mass spectrometry-based proteomics empowers deep profiling of proteome and protein posttranslational modifications (PTMs) in Alzheimer's disease (AD). 5 key findings →
Design: meta-analysis Participants: 12,017 Evidence: high
Full summary, score breakdown and related studies → Original source
The likelihood of amyloid positivity was associated with age and APOE ε4 status. 3 key findings →
Design: meta-analysis Participants: 377 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Following reports of meningoencephalitis (overall 18/300 [6%]), immunization was stopped after one (2 patients), two (274 patients), or three (24 patients) injections. 3 key findings →
Participants: 300 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Phosphorylated tau (p-tau) species (153, 181, 217, 231) increased early in preclinical AD but were reduced with gantenerumab-mediated Aβ plaque reduction. 5 key findings →
Design: post-hoc analysis Participants: 50 Evidence: high
Full summary, score breakdown and related studies → Original source
Autopsy measures of Alzheimer's disease neuropathology have been leveraged as endophenotypes in previous genome-wide association studies (GWAS). 2 key findings →
Design: meta-analysis Participants: 2,701 Evidence: high
Full summary, score breakdown and related studies → Original source
This 2026 update is an even larger follow-up to the 2022 Bellenguez GWAS, combining data from nearly 1 million people. 5 key findings →
Design: meta-analysis Participants: 978,514 Evidence: high
Full summary, score breakdown and related studies → Original source
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
An unresolved question for the understanding of Alzheimer's disease (AD) pathophysiology is why a significant percentage of amyloid-β (Aβ)-positive cognitively unimpaired (CU) individuals do not develop detectable downstream tau pathology and, consequently, clinical deterioration. 5 key findings →
Design: cohort Participants: 1,016 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The FDA approved lecanemab for Alzheimer's disease in January 2023 which acts as a novel disease-modifying anti-amyloid-beta (Aβ) human monoclonal antibody and is administered intravenously. 5 key findings →
Design: systematic review Participants: 2,729 Evidence: high
Full summary, score breakdown and related studies → Original source
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
Concentrations of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years before expected symptom onset. 5 key findings →
Design: cross-sectional Participants: 128 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
GWAS of Alzheimer's disease have been predominantly based on European ancestry cohorts with clinically diagnosed patients. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
EQW affected FCN2 (Cohen's d -0.019), PAI-1 (Cohen's d -0.033), sVCAM-1 (Cohen's d 0.035) and a cytokine-cytokine cluster (Cohen's d 0.037) significantly compared with placebo. 4 key findings →
Participants: 13,752 Evidence: low
Full summary, score breakdown and related studies → Original source
Although recent clinical trials targeting amyloid-β in Alzheimer's disease have shown promising results, there is increasing evidence suggesting that understanding alternative disease pathways that interact with amyloid-β metabolism and amyloid pathology might be important to halt the clinical deterioration. 4 key findings →
Design: longitudinal study Participants: 75 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study Participants: 3,397 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Compelling experimental evidence suggests that microglial activation is involved in the spread of tau tangles over the neocortex in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 130 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
77/100
A total of 17 articles were identified. Plasma Aβ42/40 ratio was inversely correlated with aPET positivity r = -0.48 (95% confidence interval (CI): -0.65--0.31). 5 key findings →
Design: systematic review Participants: 17 Evidence: high
Full summary, score breakdown and related studies → Original source
Synthesis methods We meta-analysed results for each outcome within each comparison using the inverse variance method and the random-effects model. 5 key findings →
Design: meta-analysis Participants: 20,342 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In BioFINDER-2, the mean (SD) age was 65.7 (14.4) with 261 females (52.7%). 3 key findings →
Design: cohort Participants: 983 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The neuropathological confirmation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles (NFT) remains the gold standard for a definitive diagnosis of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 115 Evidence: moderate
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 →