No amyloid-related imaging abnormalities occurred. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
A total of 64 patients were enrolled in this ongoing real-world study. 5 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ε4 noncarriers and those with lower baseline amyloid burden. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Patients (N = 2,512) receiving lecanemab infusion had a mean age of 75.4 (standard deviation = 5.7) years as compared to 80.8 (8.9) years in patients with MCI/AD not receiving the infusion. 5 key findings →
Participants: 2,512 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study underscores the importance of vigilant monitoring for ARIA and other neurologic and psychiatric AEs associated with lecanemab in real-world clinical settings. 4 key findings →
Participants: 1,307,937 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundLecanemab is the first approved disease-modified therapy in Japan for patients with mild cognitive impairment (MCI) due to Alzheimer's disease (AD) or mild AD dementia (AD-D).ObjectiveThis study aims to evaluate the social value of lecanemab in Japan. 1 key finding →
Design: modelling Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab is a humanized monoclonal antibody that binds soluble brain amyloid-β protein, promoting its removal and slowing the underlying process of Alzheimer disease. 1 This mechanism aligns with the amyloid hypothesis, a debated model of Alzheimer disease pathogenesis.1 Only patients with mild cognitive impairment (MCI) or mild dementia due to Alzheimer disease are eligible for lecanemab treatment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab, an amyloid-targeting monoclonal antibody, was recently approved for early symptomatic Alzheimer's disease in South Korea. 5 key findings →
Participants: 112 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Within the limitations of measuring in vitro equilibrium binding activity of in‐house recombinant antibodies to aqueously extracted Aβ from human postmortem brain tissue, we could not discern a population of Aβ aggregates ( e.g . protofibrils) accessible to one antibody but not the other two. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The anti-amyloid monoclonal antibody lecanemab received the US accelerated approval for mild cognitive impairment or mild dementia stage of Alzheimer disease in January 2023, which was converted into traditional approval in June 2023. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our results show that lecanemab exhibits high binding affinity to amyloid-β fibril structures that have a flexible N-terminus in common, as is the case for type I, type II and murine type III amyloid-β fibril polymorphs, which resemble or are identical to human structures observed in sporadic and familial cases of Alzheimer's disease, including a case with the Arctic (E22G) mutation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
-glycans found at the N304 site of lecanemab of the heavy chain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Zusammenfassung Die Alzheimer Krankheit (AD) ist eine schwere und fortschreitende neurodegenerative Erkrankung des Gehirns, die bislang mit primär nur symptomatisch wirksamen medikamentösen und nicht-medikamentösen Therapieformen als Standardtherapie behandelt wird. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ε4 heterozygous woman with mild cognitive impairment and CSF biomarker evidence of AD underwent treatment with intravenous lecanemab. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
35/100
Alzheimer’s disease (AD), the leading cause of dementia, is a multifaceted neurodegenerative disorder characterized by amyloid-beta (Aβ) aggregation, tau pathology, and neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Monoclonal antibodies such as lecanemab and donanemab show reduction in amyloid plaque and slowing of cognitive and functional decline (modest) in early AD (mild cognitive impairment or mild dementia). 5 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Monoclonal antibodies such as lecanemab and donanemab show reduction in amyloid plaque and slowing of cognitive and functional decline (modest) in early AD (mild cognitive impairment or mild dementia). 5 key findings →
Design: narrative review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
La hipótesis amiloide, que propone la acumulación del péptido ?-amiloide (?A) en la sinapsis, es el factor clave de la patogénesis de la enfermedad de Alzheimer (EA) y esta ha sido la idea dominante en el campo de la investigación de la EA durante casi 30 años. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28/100
Canada’s Drug Agency (CDA-AMC) recommends that Leqembi be reimbursed by public drug plans for the treatment of adult patients in the early stages of Alzheimer disease (AD) (i.e., mild cognitive impairment [MCI] or mild dementia) who have evidence of amyloid in the brain and who are APOE epsilon 4 (APOE4) noncarriers or heterozygotes, if certain conditions are met. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Este ensayo tiene como objetivo analizar la eficacia del lecanemab como terapia modificadora de la enfermedad de Alzheimer (EA). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Introducción: la enfermedad de Alzheimer (EA) se define como un trastorno neurodegenerativo caracterizado por acumulación de placas beta amiloide a nivel cerebral, lo cual ocasiona alteraciones histopatológicas y se manifiesta, principalmente, en el deterioro cognitivo (DC).Objetivo: evaluar el efecto de lecanemab sobre el DC en pacientes con EA.Material y métodos: metaanálisis de artículos originales que evaluaron el DC durante los periodos de intervención con placebo y lecanemab. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
La Agencia Europea de Medicamentos (EMA), tras realizar su comité CHMP una nueva evaluación de su dictamen inicial negativo en julio 2024, ha recomendado que se otorgue una autorización de comercialización limitada a pacientes de Alzheimer, que tienen una o ninguna copia de ApoE4, una determinada forma del gen de la proteína apolipoproteína E. Esta población tiene menos probabilidades de experimentar anomalías de imagen relacionadas con el amiloide (ARIA), una reacción adversa grave conocida, que implica edema (hinchazón) y posibles hemorragias cerebrales. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although monoclonal antibodies targeting amyloid provide small benefits on cognitive and functional scales in patients with Alzheimer dementia, these improvements are far below the MCID for each outcome and are accompanied by clinically meaningful harms. 2 key findings →
Design: meta-analysis Participants: 23,202 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
65/100
Alzheimer's disease (AD) therapies utilizing amyloid-β (Aβ) immunization have shown potential in clinical trials. 2 key findings →
Design: case-control Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
Indeed, in our review, we observed a stage-dependent neuroinflammatory process in the AD brain. 2 key findings →
Design: longitudinal study 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.
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 →