27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In the pivotal study in the overall population, the treatment showed a difference of −0.45 points between lecanemab and placebo in the adjusted mean change from baseline on the Clinical Dementia Rating Scale Sum of Boxes (CDR-SB) at 18 months (the primary endpoint). 5 key findings →
Design: clinical trial Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Based on the stakeholder responses from fifteen providers and twenty community members, there was strong consensus in the need for local brain health services. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A Cognitive Task Force (CTF) was established for the MissionAD program with the aim of reducing the screen failure (SF) rate to ∼30% and thereby reduce unnecessary subject burden, site burden, and excess trial costs. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To the Editor: We have recently highlighted the potential pitfalls of amyloid-beta (Aβ) PET, suggesting that both Aβ and tau assessments are necessary to relate clinical symptoms to Alzheimer disease (AD) pathology.1 Herein, we would like to present 3 additional cases related to the clinical practice of disease-modifying therapy (DMT) for AD. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The number of dementia cases continues to increase with Alzheimer's disease as the leading cause. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Genetic linkage studies suggest that Alzheimer's disease (AD) is genetically heterogeneous and that in several early onset families the disease locus is close to the amyloid precursor protein (APP) gene on chromosome 21. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
On June 7, 2021, the US Food and Drug Administration (FDA) approved aducanumab, a monoclonal amyloid targeting β-amyloid, for the treatment for Alzheimer's disease (AD). 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The Phase 2a TOGETHER trial tested bepranemab, an antibody targeting the tau protein (rather than amyloid), in 466 people with prodromal-to-mild Alzheimer's disease over 80 weeks. 3 key findings →
Design: phase-2-trial Participants: 466 Evidence: early
Full summary, score breakdown and related studies → Original source
Trontinemab is designed with a molecular 'shuttle' that helps it cross into the brain more efficiently than older anti-amyloid antibodies, aiming for faster plaque removal at lower doses. 5 key findings →
Design: phase-2-trial Participants: 13 Evidence: early
Full summary, score breakdown and related studies → Original source
Mivelsiran takes a completely different approach from antibody drugs: it's injected into the spinal fluid and uses RNA interference to tell brain cells to make less of the amyloid precursor protein in the first place, rather than clearing plaques after they form. 5 key findings →
Design: phase-1-trial Participants: 19 Evidence: preliminary
Full summary, score breakdown and related studies → Original source
This was the pivotal, large-scale trial meant to prove whether simufilam, a controversial experimental Alzheimer's drug, actually works. 5 key findings →
Design: phase-3-trial Participants: 804 Evidence: null result
Full summary, score breakdown and related studies → Original source
The results presented are sufficiently encouraging to recommend that the DEMQOL instruments be used alongside a generic measure such as the European Quality of Life-5 Dimensions (EQ-5D) in future studies of interventions in dementia as there was evidence that they can be more sensitive for patients at the milder end of disease and some limited evidence that the person with dementia measure may be able to reflect deterioration. 2 key findings →
Design: clinical trial Participants: 644 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The author panel systematically reviewed available clinical trial data detailing aducanumab use in individuals with early symptomatic Alzheimer disease. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E4 (APOE4) is a major risk factor for Alzheimer’s disease (AD). 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
In this cohort, APOE ε4 carrier status was related to disease severity at baseline rather than to the rate of cognitive decline over 80 weeks. 3 key findings →
Design: clinical trial Participants: 370 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The complete absence of ARIA distinguishes XPro1595 from amyloid-targeting therapies and supports its potential for use in combination strategies and potentially for those at a higher risk of ARIA. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have moved rapidly from metabolic medicine into neurology, but the evidence to mid-2026 refuses to resolve into a single narrative of neuroprotection. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Recent advances in blood-based biomarkers have transformed the early diagnosis of Alzheimer’s disease (AD), enabling the identification of biological risk at preclinical and presymptomatic stages in a noninvasive and accessible manner. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
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
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.
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.
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 →