27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In patients treated up to 36 months, amyloid plaque levels continued to decrease in a dose- and time-dependent manner, with levels in the 10 mg/kg fixed-dose group reaching and remaining below a quantitative cut-point discriminating a positive/negative scan. 1 Reduced amyloid plaque levels were also observed in patients switched from placebo to aducanumab during the LTE. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
PET amyloid levels were consistent with sparse-to-no neuritic amyloid-β plaques in 51% of patients after 2 years of therapy. 3 key findings →
Design: clinical trial Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source
Therapeutic antibodies have been developed to target amyloid-beta (Aβ), and some of these slow the progression of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The emergence of the United States Food and Drug Administration (FDA)-approved amyloid-targeting therapies for Alzheimer's disease challenges clinicians and healthcare providers with a transformative landscape. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This QSP platform could support clinical practice challenges to optimize real-world treatment paradigms for new and existing amyloid drugs. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With the advent of the first disease-modifying, anti-amyloid β-directed passive immunotherapy for Alzheimer's disease, questions arise who, when, and how to treat. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by cognitive decline and functional impairment, primarily driven by the accumulation of amyloid-beta (Aβ) plaques and tau tangles. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The US Food and Drug Administration (FDA)'s recent accelerated approval of two anti-amyloid antibodies for treatment of Alzheimer's disease (AD), aducanumab and lecanemab, has caused substantial debate. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
N/A. ENGAGE and EMERGE are Phase 3 clinical trials designed to confirm the clinical efficacy and safety profile of aducanumab in individuals with Early AD. 1 key finding →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Nonclinical data indicate that ACU193 can reduce the toxic effects of amyloid β oligomers. 3 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Antiamyloid antibodies have been used to reduce cerebral amyloid-beta (Aβ) load in patients with Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Given the acknowledged lack of success in Alzheimer's disease (AD) drug development over the past two decades, the objective of this review was to derive key insights from the myriad failures to inform future drug development. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lecanemab can be administered without titration with modest incidence of ARIA. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid hypothesis has been the dominant framework for Alzheimer's disease (AD) research, including the development of anti-AD therapies. 2 key findings →
Participants: 196 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-related imaging abnormalities (ARIA), side effects of anti-amyloid drugs seen in magnetic resonance imaging of the brain, are a major safety concern in patients with Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Primary biomarker efficacy endpoints were not statistically significant in either dose group. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Aducanumab is the first FDA-approved amyloid-lowering immunotherapy for Alzheimer's disease. 5 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
The introduction of anti-amyloid monoclonal antibodies marks a major shift in Alzheimer's disease (AD) care, moving treatment toward biological modification and reshaping diagnostic and organizational models. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by decreased amyloid-beta (Aβ) clearance, enhanced Aβ aggregation, an increased risk of amyloid-related imaging abnormalities (ARIA), and blood-brain barrier (BBB) dysfunction. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) remains the leading cause of dementia in Europe, with limited therapeutic options despite decades of research. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Initial studies suggested that IVIg contained antibodies against monomeric forms of Aβ 5. 5 key findings →
Design: open-label trial Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
Gantenerumab reduced amyloid PET load, CSF biomarkers of amyloid beta (Aβ)40, total tau (t-tau), phosphorylated tau 181 (p-tau181), neurogranin, S100 calcium-binding protein B (S100B), neurofilament light (NfL), alpha-synuclein (α-syn), neuronal pentraxin-2 (NPTX2), and plasma biomarkers of t-tau, p-tau181, p-tau217, and glial fibrillary acidic protein (GFAP) while increasing plasma Aβ40, Aβ42. vMRI showed increased reduction in whole brain volume and increased ventricular expansion, while hippocampal volume was unaffected. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The overall goal of the Alzheimer's Disease Neuroimaging Initiative (ADNI) is to optimize and validate biomarkers for clinical trials while sharing all data and biofluid samples with the global scientific community. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the last 2 years, there have been 3 successful trials of antiamyloid antibodies in Alzheimer disease (AD): aducanemab, now controversially US Food and Drug Administration-approved under the accelerated approval pathway1; lecanemab, now FDA-approved2; and donanemab, now going through the approval process.3 All 3 share a common broad mechanism, that is, antibody-mediated removal of β-amyloid (Aβ) from the brain, and this is almost certainly the basis of their therapeutic action.4 When used in the earliest symptomatic stages of AD, all have modest clinical effects, all clear Aβ from the brain, and all show evidence for some changes in molecular markers believed to be downstream of Aβ accumulation in keeping with disease modification.4 However, all these drugs-and several other antiamyloid immunotherapies that failed to show positive effects in clinical trials (e.g. bapineuzemab and gantenerumab)5,6-have the troubling adverse event of antibody-related imaging abnormalities (ARIA). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Host responses to anti-amyloid-β (Aβ) antibody therapy are evident in neuroimaging changes and clinical symptoms in a subset of clinical trial subjects receiving such therapy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 332 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →