Alzheimer’s disease (AD) represents a progressively growing worldwide public health burden. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
16/100
Our experiments revealed that nAβ expressing animals exhibit a unique loss of positively correlated neuron connectivity, premature disruption of system wide dynamics, and reduced overall neuronal activity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a progressive neurodegenerative disorder affecting over 55 million people worldwide, with no disease-modifying treatments currently approved. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
H. cheirifolia phenolic extracts exhibit potent, mechanism-specific antioxidant activity and promising AChE inhibition, validating traditional use in neurological complaints. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A bstract INTRODUCTION Treatment response in Alzheimer’s disease (AD) varies substantially across patients, yet no validated frameworks exist to estimate heterogeneous treatment effects (HTE) from observational data while controlling for confounding bias. 2 key findings →
Participants: 4,049 Evidence: low
Full summary, score breakdown and related studies → Original source
High placebo response is an obstacle in developing drugs to treat agitation in Alzheimer’s disease (AAD), a prevalent and burdensome symptom. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings confirm the diagnostic value of urinary β-amyloid protein detection in MCI and AD-related dementia. 5 key findings →
Design: case-control study Participants: 51,187 Evidence: high
Full summary, score breakdown and related studies → Original source
Overall, these findings indicate that use of SLCP exerts neuroprotective properties by decreasing amyloid plaque burden, preventing neuronal death, and preserving dendritic spine density and synaptic markers in the 5xFAD mice. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although the first generation of immunotherapies for Alzheimer’s disease (AD) are now clinically approved, amyloid-related imaging abnormalities (ARIA) remain a major safety problem for this class of drugs. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The administration of mAbs that specifically target the N-terminus of Aβ showed promising results in reducing Aβ burden and ameliorating cognitive decline. 5 key findings →
Design: systematic review Participants: 34 Evidence: high
Full summary, score breakdown and related studies → Original source
Amyloid-related imaging abnormalities (ARIA) remain the principal safety concern limiting adoption of anti-amyloid therapies such as lecanemab, yet their underlying biology is poorly defined. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Apolipoprotein E (APOE) e4 and e2 alleles are respectively the most risk increasing and risk decreasing, common genetic risk factors for Alzheimer’s disease (AD) 1,2 . 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We report the case of an elderly woman in good general health aside from early-stage Alzheimer’s disease who was enrolled in a randomized controlled trial of the novel therapeutic monoclonal antibody lecanemab where she was treated with the placebo, and subsequently in the open label extension study where she received lecanemab infusions every two weeks. 4 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source
After Aβ immunotherapy, capCAA was increased, likely reflecting the drainage of soluble Aβ towards the vasculature and providing a potential mechanism to disrupt AQP4-containing astrocyte endfeet, resulting in ARIA-E. We did not identify alterations in AQP4, potentially because of limitations in the timing of the post-mortem analysis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The FDA gave lecanemab (Leqembi) accelerated approval based on Phase 2 data showing it reduced amyloid plaque in the brain, ahead of full Phase 3 results. 3 key findings →
Design: regulatory decision Evidence: early
Full summary, score breakdown and related studies → Original source
The FDA approved donanemab (Kisunla) as a monthly IV infusion for people with early symptomatic Alzheimer's disease (mild cognitive impairment or mild dementia) with confirmed amyloid plaques. 3 key findings →
Design: regulatory decision Evidence: moderate
Full summary, score breakdown and related studies → Original source
The EMA's human medicines committee (CHMP) initially refused to approve lecanemab in the EU in July 2024, judging that its modest effect on cognitive decline did not outweigh ARIA risk in the broad early-Alzheimer's population studied. 3 key findings →
Design: regulatory decision Evidence: moderate
Full summary, score breakdown and related studies → Original source
The EMA initially recommended against approving donanemab in March 2025, again on ARIA risk-benefit grounds, then reversed itself after re-examination: the CHMP issued a positive opinion on July 24, 2025, and the European Commission granted marketing authorization on September 24, 2025, restricted to early-Alzheimer's patients with one or no copy of the ApoE4 gene. 3 key findings →
Design: regulatory decision Evidence: moderate
Full summary, score breakdown and related studies → Original source
The use of SLCP provides more anti-amyloid, anti-inflammatory, and neuroprotective outcomes than does Cur in the 5xFAD mouse model of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The FDA converted lecanemab (Leqembi) from accelerated to full traditional approval after the Phase 3 Clarity AD trial (1,795 patients) confirmed it slowed cognitive decline, making it the first amyloid-targeting antibody to reach full approval for Alzheimer's. The drug carries a boxed warning for ARIA, brain swelling or bleeding that is usually detected on routine MRI and is more common in people with two copies of the ApoE ε4 gene or those on blood thinners. 3 key findings →
Design: regulatory decision Evidence: moderate
Full summary, score breakdown and related studies → Original source
On January 31, 2024, Biogen announced it would discontinue development and sales of Aduhelm (aducanumab) and end the mandatory post-approval ENVISION confirmatory trial, redirecting resources to lecanemab (Leqembi) and other pipeline drugs, including two tau-targeting compounds (BIIB080, BIIB113). 3 key findings →
Design: company announcement
Full summary, score breakdown and related studies → Original source
CMS's national policy covers FDA-approved anti-amyloid monoclonal antibodies (such as lecanemab and donanemab) for Medicare patients with a documented diagnosis of mild cognitive impairment or mild Alzheimer's dementia and confirmed amyloid pathology, under a framework called 'Coverage with Evidence Development.' 3 key findings →
Design: coverage determination
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
- Randomized / 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
- Multicenter 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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,045 records (3.3% of the library) are not peer-reviewed — 966 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events
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