Alzheimer’s disease (AD) is the most common form of dementia with global burden projected to triple by 2050. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Aducanumab has recently been licensed by the Food and Drug Administration (FDA) in the USA under its ‘accelerated approval’ pathway (to provide earlier access to treatments that fulfil an unmet need based on a surrogate endpoint) for treatment of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
En junio, la Agencia de Alimentos y medicamentos de los Estados Unidos (FDA) otorgó aprobación mediante vía acelerada al medicamento aducanumab, desarrollado por Biogen, Inc. para tratamiento de la enfermedad de Alzheimer (EA). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab is a human immunoglobulin G1 anti‐amyloid beta (Aβ) antibody currently being evaluated for potential treatment of patients with early Alzheimer’s disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aducanumab, a human monoclonal antibody, was approved in June of 2021 as the first disease-modifying treatment for Alzheimer’s disease by the United States Food and Drug Administration (U.S. FDA). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Alzheimer’s disease is a major cause of morbidity and mortality. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Three new drugs are presented: dostarlimab, loncastuximab tesirine, and aducanumab. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid cascade hypothesis, according to which the self-assembly of amyloid-β peptide (Aβ) is a causative process in Alzheimer's disease, has driven many therapeutic efforts for the past 20 years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The termination of many clinical trials of amyloid-targeting therapies for the treatment of Alzheimer's disease (AD) has had a major impact on the AD clinical research enterprise. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) therapeutics based on the amyloid hypothesis have repeatedly failed in clinical trials. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
The DIAN study compared the pathophysiological markers between carriers and non-carriers of mutation for autosomal dominant Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The DIAN observational study compared the pathophysiological markers between mutation carriers and non-carriers for autosomal dominant Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Trials missing primary efficacy end points raise the question of whether the choice of drug or the limitations of disease biology were at fault. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among active and passive anti-β-amyloid (Aβ) immunotherapies for Alzheimer's disease (AD), bapineuzumab and solanezumab, two humanized monoclonal antibodies, failed to show significant clinical benefits in mild-to-moderate AD patients in large Phase III clinical trials. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, which is characterized by gradual cognitive decline associated with deterioration of daily living activities and behavioral disturbances throughout the course of the disease, is estimated to affect 27 million people around the world. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
OF THE FIELD: Alzheimer's disease is the leading cause of dementia in the elderly, and there is no disease-modifying therapy yet available. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Two new combination pediatric vaccines advancing to use in infants Oncolytic viruses successfully delivered intravenously Cuba eliminates hepatitis B among minors under 15 Alzheimer's vaccine trial a success Study: Shingles vaccine safe for patients on immune-suppressing drugs Therapeutic cancer vaccine against metastatic renal cell carcinoma enters Phase 3 Pfizer’s Men B vaccine shows promise in Phase 2 Biovest initiates formal regulatory approval process for BiovaxID in Europe 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrolysin is a peptidergic drug which displays neurotrophic action in various animal models. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Adjunctive florbetapir-PET increased quality-adjusted life years (QALYs) by 0.008 years and increased costs by 36 compared to SCE alone (incremental cost-effectiveness ratio [ICER], 4,769). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a debilitating neurodegenerative illness affecting over 35 million people worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
During the last few decades, relevant efforts have been reported to design nanocarriers for drug transport through the blood brain barrier (BBB). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Expert opinion Phase III trials showed that bapineuzumab failed to improve cognitive and functional performances in AD patients, and was associated with a high incidence of amyloid-related imaging abnormalities (ARIA). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
At the 8th International Conference on Clinical Trials in Alzheimer's Disease held November 5-7, 2015 in Barcelona, Spain, promising data were presented on two candidate Alzheimer's disease immunotherapeutic agents, gantenerumab and aducanumab. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Active or passive immunotherapy is expected to slow or stop the pathological process of Alzheimer's disease (AD). 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The problem with pure recombinant or synthetic antigens used in modern day vaccines is that they are generally far less immunogenic than older style live or killed whole organism vaccines. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
9 of the 333 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 9. The same 9 appear here every time.
- Value-Generating Exploratory Trials in Neurodegenerative Dementias
- Trial of Solanezumab in Preclinical Alzheimer's Disease
- ARIA in patients treated with lecanemab (BAN2401) in a phase 2 study in early Alzheimer's disease
- Therapeutic news in Alzheimer's disease: Soon a disease-modifying therapy?
- First-In-Human safety and long-term exposure data for AAB-003 (PF-05236812) and biomarkers after intravenous infusions of escalating doses in patients with mild to moderate Alzheimer's disease
- Alzheimer's Disease: Key Insights from Two Decades of Clinical Trial Failures
- Lecanemab for mild Alzheimer disease - is there a way forward?
- FDA-Approved Passive Immunization Treatments Against Aβ in Alzheimer's Disease: Where Are We Now?
- Safety and efficacy of active and passive immunotherapy in mild-to-moderate Alzheimer's disease: A systematic review and network meta-analysis
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →