Alzheimer's disease (AD) impacts more than half a million people worldwide, with no cure available. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) impacts more than half a million people worldwide, with no cure available. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder pathologically characterized by the accumulation of amyloid-beta (Aβ) and neurofibrillary tangles of hyperphosphorylated tau in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, the U.S. Food and Drug Administration (FDA) approved 2 anti-amyloid monoclonal antibodies, aducanumab (June 7, 2021) and lecanemab (July 6, 2023), for the treatment of Alzheimer's disease (AD) patients, and will most likely also approve a 3rd one, donanemab, soon. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hardy and Mummery discuss the recent positive findings in the clinical trial of lecanemab in early Alzheimer’s disease, and the implications for the amyloid hypothesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, the leading cause of dementia, is defined by extracellular amyloid‑β (Aβ) plaques, intracellular tau aggregates and neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anti-amyloid monoclonal antibodies have finally achieved their translational breakthrough after many years of unmet expectations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Annotation. Alzheimer’s disease (AD) is the leading cause of dementia in older adults, characterized by the accumulation of pathological proteins – beta-amyloid (Aβ) and hyperphosphorylated tau protein – resulting in neurodegeneration and cognitive impairment. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-targeting therapy has recently become widely available in the United States for the treatment of patients with symptomatic mild Alzheimer disease (AD). 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
VBPs indicate how much 174 countries should be willing to pay. 2 key findings →
Design: modelling Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Reimbursement decisions for new Alzheimer's disease (AD) treatments are informed by economic evaluations. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Two anti-amyloid monoclonal antibodies (MABs)-lecanemab (Leqembi ® ) and aducanumab (Aduhelm ® )-have been approved in the USA for the treatment of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A large body of clinical and nonclinical evidence supports the role of neurotoxic soluble beta amyloid (amyloid, Aβ) oligomers as upstream pathogenic drivers of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common chronic neurodegenerative disease worldwide. 2 key findings →
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
With recent data demonstrating that lecanemab treatment can slow cognitive and functional decline in early symptomatic Alzheimer disease (AD), it is widely anticipated that this drug and potentially other monoclonal antibody infusions targeting β-amyloid protein will imminently be realistic options for some patients with AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Antibody-mediated removal of aggregated β-amyloid (Aβ) is the current, most clinically advanced potential disease-modifying treatment approach for Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Epilepsy is a cause of profound disability in patients with Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The approvals of the first anti-amyloid antibodies for the treatment of Alzheimer's disease have changed both the clinical and research landscape for the disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Symptom-oriented treatment has been the mainstay of Alzheimer disease (AD) pharmacotherapy for decades. 4 key findings →
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
Anti-amyloid monoclonal antibodies (MABs) have introduced a new era of Alzheimer's disease (AD) therapeutics with disease-targeted drugs. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Based on "reducing amyloid plaques in the brain", the U.S. Food and Drug Administration has granted accelerated and full approval for two monoclonal anti-Alzheimer's antibodies, aducanumab and lecanemab, respectively. 3 key findings →
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
Pharmacological interventions for dementia include medications aimed at alleviating its core symptom: cognitive dysfunction. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent rejection of lecanemab by the European Medicines Agency despite its approval in other countries highlights the debate among researchers and regulatory bodies about the efficacy, safety, and underlying scientific basis of drugs to treat Alzheimer’s disease. [Image: see text] 1 key finding →
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 →