30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Treatment options for Alzheimer disease (AD) are limited and have focused mainly on symptomatic therapy and improving quality of life. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individuals with Down syndrome (DS) have a genetically determined form of Alzheimer's disease (AD) due to the amyloid precursor protein (APP) gene dose effect. 1 key finding →
Design: longitudinal study Evidence: moderate
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Alzheimer's disease (AD) is the leading cause of dementia, presenting a significant unmet medical need worldwide. 4 key findings →
Evidence: low
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A total of 282 participants were followed for an average of 2.9 years (standard deviation [SD] 1.3 years). 5 key findings →
Participants: 282 Evidence: low
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This special issue of Alzheimer's & Dementia celebrates the accomplishments of the Alzheimer's Disease Neuroimaging Initiative (ADNI) project as it approaches its 20th anniversary in 2024, supported by funding from the National Institute on Aging. 1 key finding →
Design: longitudinal study Evidence: moderate
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Second-generation anti-amyloid monoclonal antibodies are emerging as a viable therapeutic option for individuals with prodromal and mild dementia due to Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Alzheimer's disease (AD) is a complex and progressive neurodegenerative disorder with a continuum of stages ranging from preclinical/asymptomatic phase to severe dementia. 1 key finding →
Evidence: low
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Treatments for neurodegenerative disorders remain rare, but recent FDA approvals, such as lecanemab and aducanumab for Alzheimer disease (MIM: 607822), highlight the importance of the underlying biological mechanisms in driving discovery and creating disease modifying therapies. 4 key findings →
Evidence: low
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Of 1309 new patients, 514 (39% of new patients) had clinical mild cognitive impairment (MCI) or AD. 5 key findings →
Participants: 1,309 Evidence: low
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Alzheimer is an irreversible progressive neurodegenerative disease that causes failure of cerebral neurons and disability of the affected person to practice normal daily life activities. 4 key findings →
Evidence: low
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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
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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
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VBPs indicate how much 174 countries should be willing to pay. 2 key findings →
Design: modelling Evidence: moderate
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Reimbursement decisions for new Alzheimer's disease (AD) treatments are informed by economic evaluations. 3 key findings →
Evidence: moderate
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We question the validity of the evidence for the removal of amyloid in particular as assessed by amyloid PET imaging, believing that what is observed is more likely a large nonspecific amyloid PET signal in the white matter that diminishes during immunotherapy-in line with dose-dependent increases in amyloid-related imaging abnormalities and increased loss of cerebral volume in treated compared with placebo patients. 1 key finding →
Evidence: low
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Established drug therapies for Alzheimer disease (cholinesterase inhibitors and memantine) do not modify the disease course and provide only modest clinical benefit. 4 key findings →
Evidence: low
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A total of 85 patients were included in the study with rare genotypes excluded from analysis (3 patients). 5 key findings →
Participants: 85 Evidence: moderate
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In the base-case analysis from the healthcare perspective, SoC was more clinically effective than BSC with a cost per QALY of $5211. 3 key findings →
Evidence: low
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All recently approved monoclonal antibodies (eg, aducanumab, lecanemab, and donanemab) for Alzheimer disease (AD) were shown to increase the risks of amyloid-related imaging abnormalities (ARIA) in randomized clinical trials, which can include brain swelling or hemorrhage. 4 key findings →
Participants: 240 Evidence: high
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A total of 143 patients with cognitive concerns were included who underwent a PrecivityAD2 test as part of their clinical evaluation. 5 key findings →
Participants: 4,000 Evidence: moderate
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Although β-site APP-cleaving enzyme 1 (BACE1) and secretase inhibitors did not achieve success in clinical trials because of mechanism-based toxicity and cognitive impairment, new monoclonal antibodies such as lecanemab and donanemab have shown high amyloid plaque clearance and reduced cognitive deterioration. 5 key findings →
Evidence: low
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In 4 of 5 patients treated with lecanemab or donanemab and who had moderate or severe ARIA-E, Aβ PET signal decreased significantly more in regions that had been involved with ARIA-E. Greater regional Aβ PET signal reduction in areas involved by ARIA-E may reflect enhanced local Aβ clearance, reduced tracer binding site availability, impaired glymphatic flow from immune complex deposition, or other mechanisms. 3 key findings →
Evidence: low
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The blood-brain barrier (BBB) displays a highly organized and complex structure, which is important for maintaining brain homeostasis and protecting the brain from foreign molecules or pathogens. 5 key findings →
Evidence: low
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Early diagnosis of mild cognitive impairment (MCI) and Alzheimer's disease (AD) with mild dementia is becoming increasingly important to enable patients to receive appropriate treatment with available amyloid-targeting therapies. 5 key findings →
Design: narrative review Evidence: low
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Alzheimer Disease (AD) constitutes a major global healthcare problem. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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