28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In this prospective cohort study, we included adults aged 40 years or older with subjective cognitive decline, mild cognitive impairment, or dementia, based on cognitive test results and clinical assessments, consecutively recruited at two memory clinics in Sweden, as part of the Swedish BioFINDER-2 study. 3 key findings →
Design: cohort Participants: 572 Evidence: high
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The non-linear function indicates that a higher dose is not necessarily better in multidomain interventions. 3 key findings →
Design: randomized controlled trial Participants: 749 Evidence: high
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In this study, quantitative results were inconclusive owing to small sample size. 5 key findings →
Design: randomized controlled trial Participants: 25 Evidence: high
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Using stratification with simply assessed markers, it is now not only possible, but practical to include patients with RBD in neuroprotective trials against Parkinson disease, multiple system atrophy, and dementia with Lewy bodies. 3 key findings →
Design: prospective cohort Participants: 89 Evidence: moderate
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The literature has several methodological limitations including lack of sufficient algorithm development descriptions and standard definitions. 1 key finding →
Participants: 255 Evidence: moderate
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We analyzed 1,240 MRIs from 473 patients (age: 69.2 ± 7.4 [range: 49-87]; 32.8% women). 2 key findings →
Design: cohort study Participants: 1,240 Evidence: moderate
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Benzodiazepine use is associated with an increased risk of Alzheimer's disease. 3 key findings →
Design: case-control study Participants: 1,796 Evidence: moderate
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There were 838 BioFINDER-2 participants (mean age, 73.9 [SD, 7.3] years; 431 women [51%]; 407 men [49%]) and 380 ADNI participants (average age, 72.9 [SD, 7.0] years; 194 women [51%]; 186 mean [49%]) included. 3 key findings →
Design: cross-sectional Participants: 838 Evidence: moderate
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Their results on motor testing from the preceding years were plotted, and then assessed with regression analysis, to determine when markers first deviated from normal values. 3 key findings →
Design: cohort study Participants: 78 Evidence: moderate
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This study aimed to determine the extent to which cognitive measures can predict progression from mild cognitive impairment (MCI) to Alzheimer's type dementia (AD), assess the predictive accuracy of different cognitive domain categories, and determine whether accuracy varies as a function of age and length of follow-up. 5 key findings →
Design: longitudinal study Participants: 2,365 Evidence: moderate
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Prospective cohort study with 5 years of follow-up. 4 key findings →
Design: cohort study Participants: 154 Evidence: moderate
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Parkinson's disease has a long prodromal stage with various subclinical motor and non-motor manifestations; however, their evolution in the years before Parkinson's disease is diagnosed is unclear. 5 key findings →
Design: longitudinal study Evidence: moderate
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This comprehensive portrait of rural-urban differences in dementia care highlights possible geographically based inequities and can be used by researchers and decision makers to guide development of more equitable dementia care policies. 2 key findings →
Design: systematic review Evidence: high
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The pooled sample comprised 4657 participants (30% women) aged ≥ 60 years (mean age was 74 years at sleep assessment). 5 key findings →
Design: cohort study Participants: 2,374 Evidence: moderate
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Using the Swedish BioFINDER-2 cohort [n = 1702, 50.7% male, mean (standard deviation) age 68.4 (12.2) years], we compared the associations between tau/Aβ-PET load and fluid biomarkers alone versus biomarkers in a ratio with a reference protein (Aβ40 or np-tau) in univariate linear regression models. 5 key findings →
Design: longitudinal study Participants: 1,702 Evidence: moderate
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Co-pathology is a common feature of neurodegenerative diseases that complicates diagnosis, treatment and clinical management. 4 key findings →
Design: cross-sectional Participants: 17,187 Evidence: early
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Although we have found a slightly lower risk than other reports, the risk of developing neurodegenerative disease in idiopathic REM sleep behavior disorder is substantial, with the majority of patients developing Parkinson disease and Lewy body dementia. 2 key findings →
Participants: 113 Evidence: low
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Reducing the risk of dementia can halt the worldwide increase of affected people. 1 key finding →
Evidence: low
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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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Cardiovascular autonomic dysfunction, REM sleep behavior disorder, color discrimination ability, and gait dysfunction strongly predict development of dementia in Parkinson disease. 1 key finding →
Participants: 80 Evidence: low
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Within the training set, individuals closer to or beyond their parent's symptom onset demonstrated reduced grey matter volume and altered functional connectivity, specifically in regions known to be vulnerable in Alzheimer's disease. 5 key findings →
Design: longitudinal study Participants: 138 Evidence: moderate
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Long-term use of urate-lowering therapies (ULT) may reduce inflammaging and thus prevent cognitive decline during aging. 3 key findings →
Design: randomized controlled trial Participants: 51 Evidence: high
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Our findings elucidate the predictive values of environmental factors and comorbid conditions in identifying RBD patients at higher risk of phenoconversion. 4 key findings →
Participants: 319 Evidence: moderate
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White matter hyperintensities (WMHs) are neuroimaging markers widely interpreted as caused by cerebral small vessel disease, yet emerging evidence suggests that a subset may have a neurodegenerative etiology. 1 key finding →
Participants: 32,526 Evidence: moderate
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The APOE locus is the strongest genetic factor for Alzheimer's disease, with ε4 increasing and ε2 decreasing risk, yet the basis of these opposing effects remains unclear. 1 key finding →
Design: cohort Evidence: moderate
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 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.
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 →