27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Choroid plexus (ChP) is emerging as a key brain structure in the pathophysiology of neurodegenerative disorders. 4 key findings →
Design: longitudinal study Participants: 135 Evidence: moderate
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Cohort studies report inconsistent associations between body mass index (BMI) and all-cause incident dementia. 4 key findings →
Design: cohort study Participants: 322,336 Evidence: moderate
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The recent availability of longitudinal data on the possible association of different lifestyles with dementia and Alzheimer's disease (AD) allow some preliminary conclusions on this topic. 4 key findings →
Design: longitudinal study Evidence: moderate
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This longitudinal study examined whether insulin resistance among late middle-aged, cognitively healthy individuals was associated with 1) less gray matter in Alzheimer disease-sensitive brain regions and 2) worse cognitive performance. 4 key findings →
Design: longitudinal study Participants: 372 Evidence: moderate
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The study included 732 participants (median [IQR] age, 41 [34.0-48.0] years; 369 [50.4%] male; 64 [8.9%] Black or African American, 587 [81.3%] White, and 71 [9.8%] other races); 414 reported baseline FTS use and 318 did not. 5 key findings →
Design: cohort study Participants: 732 Evidence: moderate
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Sample 1 included 1656 participants (mean [range] age, 58.1 [29.7-85.6] years; 903 female [54.5%]), and sample 2 included 935 participants (mean [range] age, 67.6 [60.0-85.6] years; 518 female [55.4%]). 4 key findings →
Design: cohort study Participants: 1,656 Evidence: moderate
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A total of 450 111 participants were included in the study (mean [SD] age, 51.1 [9.8] years; 70.8% women) and followed up during a median (IQR) time of 14.9 (4.1) years. 5 key findings →
Design: cohort study Participants: 111 Evidence: moderate
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Of the 14 685 participants (7355 female [50%] and 7330 male [50%]; mean [SD] age, 73.8 [8.5] years) who met the inclusion criteria, 221 participants (1.5%) developed LOE during follow-up. 5 key findings →
Design: longitudinal study Participants: 713 Evidence: moderate
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Blood-based biomarkers for Alzheimer's disease (AD) pathology have been investigated intensively as markers for AD-related neurodegeneration. 5 key findings →
Design: cohort study Participants: 158 Evidence: moderate
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After a median follow-up time of 14.3 (7.9-20.0) years, dementia was recorded in 530 (1.2%) individuals with type 1 diabetes and 1,867 (0.9%) age-, sex-, and county-matched control individuals (mean baseline age 33.0 [14.0] years). 4 key findings →
Design: cohort study Participants: 43,440 Evidence: moderate
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Over a mean follow-up of 7.9 years, 694 incident dementia cases occurred. 5 key findings →
Design: cohort study Participants: 82,391 Evidence: moderate
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= 0.009). Significant differences in annualized changes in these FA and MD values were found depending on the presence or absence of type 2 diabetes and smoking. 4 key findings →
Design: longitudinal study Participants: 6,471 Evidence: moderate
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Based on positive/negative results on the different biomarkers, subjects were classified as 'AD-LB-' (n = 304), 'AD+LB-' (n = 335), 'AD+LB+' (n = 158) and 'AD-LB+' (n = 68). 5 key findings →
Design: longitudinal study Participants: 661 Evidence: moderate
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Among 2556 patients (mean age 79 ± 9 years; 56% women), delirium occurred in 957 (37%). 5 key findings →
Design: cohort study Participants: 2,556 Evidence: moderate
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This study classified preclinical Alzheimer's disease (AD) using cognitive screening, neighborhood deprivation via the area deprivation index (ADI), and sociodemographic and genetic risk factors. 2 key findings →
Design: longitudinal study Participants: 2,792 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings illuminate the potential benefits of ChEI treatment in DLB patients. 4 key findings →
Design: cohort Participants: 1,095 Evidence: moderate
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Previous studies have suggested that the APOE ɛ4 allele plays a role in the risk and age at onset of dementia in DS; however, data on in vivo biomarkers remain scarce. 5 key findings →
Design: cohort study Evidence: moderate
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The mean (SD) age was 73.9 (7.35) years among the 237 ADNI participants and 70.2 (9.7) years among the 130 Avid-A05 participants. 2 key findings →
Design: cohort study Participants: 237 Evidence: moderate
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Among cognitively normal participants with positive biomarkers, 34.4% developed cognitive impairment (Clinical Dementia Rating > 0) as compared to 8.4% of those with negative biomarkers. 2 key findings →
Design: longitudinal study Participants: 720 Evidence: moderate
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Higher levels of P-tau181 (HR = 1.32 [95% CI: 1.17-1.51]), NfL (HR = 1.19 [95% CI: 1.03-1.36]), and GFAP (HR = 1.36 [95% CI: 1.22-1.52]), and a lower Aβ42/Aβ40 ratio (HR = 0.80 [95% CI: 0.68-0.95]) were associated with an increased risk of progressing to clinically-diagnosed DAT. 2 key findings →
Design: longitudinal study Participants: 1,007 Evidence: moderate
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Both participant and study partner CFI increased over the duration of the study indicating worsening cognitive functioning. 3 key findings →
Design: longitudinal study Participants: 1,147 Evidence: moderate
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Mean (SD) follow-up was 4.8 (2.6) years. 3 key findings →
Design: cohort study Participants: 298 Evidence: moderate
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Our findings indicate that tau accumulates even in amyloid-negative healthy OA and this process can be measured with in vivo tau-PET. 5 key findings →
Design: longitudinal study Evidence: moderate
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Better sleep consolidation attenuates the effect of APOE genotype on incident AD and development of neurofibrillary tangle pathology. 2 key findings →
Design: cohort study Participants: 698 Evidence: moderate
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During follow-up 319 participants developed dementia (221 had AD). 4 key findings →
Design: cohort study Participants: 2,288 Evidence: moderate
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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →