31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Key results included a 35% slowing of decline on the Integrated Alzheimer's Disease Rating Scale (iADRS) and a 36% slowing on the Clinical Dementia Rating-Sum of Boxes (CDR-SB). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Aducanumab is a monoclonal antibody selective for amyloid β (Aβ) aggregates. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid cascade hypothesis is a useful framework for therapeutic development in Alzheimer's disease (AD). 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Selecting the right dose is a significant challenge in designing clinical development programs, especially for slowly progressing diseases lacking predictive biomarkers of efficacy that may require long-term treatment to assess clinical benefit. 2 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source
Donepezil has psychotropic properties, and pretreatment behaviors help predict patients' responses to treatment. 4 key findings →
Design: open-label trial Participants: 86 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-β (Aβ) plaques and neurofibrillary tangles containing phosphorylated tau protein are major hallmarks of Alzheimer's disease (AD). 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia, which is characterized by a progressive neurodegenerative disorder that is extremely difficult to treat and severely reduces quality of life. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is pathologically characterized by deposition of amyloid plaques (comprising amyloid β [Aβ] protein) and neurofibrillary tangles (comprising tau protein), and neuronal death. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Three deaths have been reported related to treatment with lecanemab.6 Patients receiving DMT require frequent monitoring with MRI brain scans (four or more per year), as there is a high rate of clinically significant amyloid-related imaging abnormalities (ARIA), both brain oedema (ARIA-E) and macro- and microhaemorrhages (ARIA-H). 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-targeting therapies represent the first validated disease-modifying strategy for AD but are not definitive solutions. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Lecanemab should only be prescribed for patients with MCI due to AD or mild AD dementia following careful clinical evaluation confirming AD pathology, with caution exercised in patients at increased ARIA risk (e.g. APOEε4 gene carriers). 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Many insults, including trauma, ischemia, infection, inflammation, and neurodegeneration, result in irreversible damage to the central nervous system. 3 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Progress in understanding the complexity of Alzheimer's disease informs the search for combination therapies that can successfully prevent or substantially slow the progression of the disease. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Aducanumab, a human-derived antibody targeting amyloid-β (Aβ), is in Phase 3 clinical trials for the treatment of Alzheimer's disease. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Development of disease-modifying treatments for Alzheimer's disease (AD) has been challenging, with no drugs approved to date. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
In the A4 study, solanezumab did not reduce the decline in cognition or function and had no effect on brain amyloid burden. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The results from the gantenerumab phase 3 programs are expected by the end of 2022 and will add critical information to the collective knowledge on the search for effective AD treatments. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The results of the aducanumab studies have not been published in peer-reviewed form and both the analysis presented by Dr Knopman and collaborators and this perspective are based on data presented in 2019 at the Clinical Trials in AD (CTAD) meeting3; both discussions must be seen as tentative until full data are available. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The symptomatic drugs currently on the market for Alzheimer's disease (AD) have no effect on disease progression, and this creates a large unmet medical need. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
An international task force of investigators from academia, industry, nonprofit foundations, and regulatory agencies met in Monte Carlo, Monaco, on October 31, 2012, to review lessons learned from the recent bapineuzumab and solanezumab trials, and to incorporate insights gained from these trials into future clinical studies. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Based on the data to date, it is difficult to accurately assess the role of aducanumab in patients with MCI or mild AD. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The start of the new year signals that it is time for mAbs' annual review of the therapeutic monoclonal antibodies (mAbs) in active Phase 2/3 or Phase 3 clinical studies. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
These therapies are based on the assumption that Aβ accumulation is the primary pathogenic trigger of AD. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
High-dose vitamin supplementation reduces homocysteine levels in patients with AD. 2 key findings →
Design: open-label trial Participants: 69 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Patients with early symptomatic Alzheimer's disease showed less cognitive and functional decline with donanemab compared with placebo in a Phase 2 study offering up to 72 weeks of treatment. 3 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 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.
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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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