27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
A single-question screen for RBD may reliably detect disease, with psychometric properties favorably comparable to those reported for longer questionnaires. 2 key findings →
Design: case-control study Evidence: moderate
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Blood-based AD biomarker concentrations are associated with pathological and clinical diagnoses and can predict future development of clinical AD, providing evidence that they can be incorporated into multi-ethnic, community-based studies. 3 key findings →
Evidence: low
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Neuronal intranuclear inclusion disease (NIID) is a slowly progressive neurodegenerative disease characterized by eosinophilic hyaline intranuclear inclusions in the central and peripheral nervous system, and also in the visceral organs. 1 key finding →
Participants: 57 Evidence: low
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The Alzheimer center of the VU University Medical Center opened in 2000 and was initiated to combine both patient care and research. 2 key findings →
Participants: 6,000 Evidence: moderate
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APOE genotyping does not provide sufficient sensitivity or specificity to be used alone as a diagnostic test for Alzheimer's disease, but when used in combination with clinical criteria, it improves the specificity of the diagnosis. 5 key findings →
Participants: 2,188 Evidence: low
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The current study is a controlled clinical investigation of two nonpharmacological treatments of depression in patients with Alzheimer's disease. 4 key findings →
Evidence: low
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Based on informant report, disturbed arousal and disorganized speech are specific aspects of fluctuations in dementia with Lewy bodies that reliably distinguish dementia with Lewy bodies from Alzheimer's disease and normal aging. 4 key findings →
Participants: 200 Evidence: low
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In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. 5 key findings →
Evidence: low
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Clinical and neuropathologic evidence points to the development of Alzheimer's disease (AD) in seven Down's syndrome patients above age 40. 3 key findings →
Design: longitudinal study Evidence: moderate
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Current criteria for the clinical diagnosis of pathologically confirmed corticobasal degeneration (CBD) no longer reflect the expanding understanding of this disease and its clinicopathologic correlations.
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This randomized clinical trial found that ADRD screening in PC was not associated with improvement in family member health-related quality of life, caregiver preparedness, or caregiving self-efficacy. 5 key findings →
Design: RCT Participants: 1,808 Evidence: null result
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MCI as an entity is evolving and somewhat controversial. 1 key finding →
Participants: 93 Evidence: low
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Alzheimer's disease is the most common cause of dementia in elderly people. 5 key findings →
Evidence: high
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On the basis of their findings in this large community population of elderly people, the authors conclude that a wide range of dementia-associated mental and behavioral disturbances afflict the majority of individuals with dementia. 3 key findings →
Participants: 5,092 Evidence: low
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Participants: 108 Evidence: low
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For one of the primary analyses, the interpretation of the florbetapir scans (majority interpretation of five nuclear medicine physicians, who classified each scan as amyloid positive or amyloid negative) was compared with amyloid pathology (assessed according to the Consortium to Establish a Registry for Alzheimer's Disease standards, and classed as amyloid positive for moderate or frequent plaques or amyloid negative for no or sparse plaques); correlation of the image analysis results with amyloid burden was tested as a coprimary endpoint. 3 key findings →
Participants: 59 Evidence: low
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To be diagnostically useful, structural MRI must reliably distinguish Alzheimer's disease (AD) from normal aging in individual scans. 1 key finding →
Evidence: low
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Each measure independently predicted a diagnosis of dementia. 1 key finding →
Participants: 2,885 Evidence: low
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Longitudinal changes in motor function may be useful in the early detection of dementia during preclinical stages, when the utility of disease-modifying therapies would be greatest. 1 key finding →
Design: cohort study Evidence: moderate
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Neuroimaging and biofluid tau markers hold potential for optimising such clinical trials by augmenting participant selection, providing evidence of target engagement, and monitoring treatment efficacy. 5 key findings →
Design: clinical trial Evidence: low
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Patients with behavioural Alzheimer's disease showed worse memory scores than behavioural variant frontotemporal dementia and did not differ from typical Alzheimer's disease, while executive function composite scores were lower compared to behavioural variant frontotemporal dementia and typical Alzheimer's disease. 3 key findings →
Participants: 17 Evidence: low
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Different biomarkers for Alzheimer disease provide different information from one another that is likely to be complementary. 1 key finding →
Participants: 34 Evidence: low
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Linking the ADAMS dementia clinical assessment data to the wealth of available longitudinal HRS data on health, health care utilization, informal care, and economic resources and behavior, will provide a unique opportunity to study the onset of CIND and dementia in a nationally representative population-based sample, as well as the risk factors, prevalence, outcomes, and costs of CIND and dementia. 5 key findings →
Design: longitudinal study Participants: 856 Evidence: moderate
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Prevalence of dementia was 8.3%. 2 key findings →
Design: cross-sectional Participants: 1,238,895 Evidence: low
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We aimed to determine the regional pattern of brain atrophy associated with the C9ORF72 gene mutation, and to determine which regions best differentiate C9ORF72 from subjects with mutations in tau and progranulin, and from sporadic frontotemporal dementia. 5 key findings →
Participants: 76 Evidence: low
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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 →