30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
We included 730 Alzheimer's Disease Neuroimaging Initiative (ADNI) participants without dementia (282 cognitively normal, 448 mild cognitive impairment) with baseline [ 18 F]florbetapir PET and CSF Aβ 42 available. 4 key findings →
Design: longitudinal study Participants: 318 Evidence: moderate
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The relationship between mild behavioral impairment (MBI) and Alzheimer's disease (AD) is intricate and still not well investigated. 4 key findings →
Design: longitudinal study Participants: 1,129 Evidence: moderate
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The mean age of participants was 77.1 years (SD = 7.6), and 2779 were women (weighted % = 56.7). 4 key findings →
Design: cohort study Participants: 1,238 Evidence: moderate
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Overall, 1.45% of the study cohort age ≥65 received HBMC. 5 key findings →
Design: longitudinal study Participants: 132,147 Evidence: moderate
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The weighted prevalence of dementia at provincial level in China in 2018 ranged from 2.62% (95%BCI: 1.70%, 3.91%) to 13.53% (95%BCI: 8.82%, 20.93%). 5 key findings →
Design: longitudinal study Participants: 17,176 Evidence: moderate
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The sample included 740 donors (417 female [56.4%]; mean [SD] age at death, 81.5 [10.3] years; mean [SD] VBI score, 0.7 [1.0]; and median life course ADI, 7.08 [IQR, 4.33-9.83]), with residential years spanning 1905 to 2018. 5 key findings →
Design: cohort study Participants: 740 Evidence: moderate
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Among 463 ADNI participants with baseline MCI (mean age 72.6 ± 7.3 years, 43.4% female), the OSA PRS, adjusted for BMI, was significantly associated with MCI-to-AD progression. 5 key findings →
Design: prospective cohort Participants: 752 Evidence: moderate
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Among 809 participants (mean [SD] age at death, 91.3 [6.1] years; 538 [72%] female; mean [SD] follow-up, 7.2 [4.4] years), HS was present in 82 (10.1%) participants; 71 participants (9%) had both HS and LATE-NC, and in the scored subset, 43 participants (14%) had moderate and 35 participants (12%) had severe hippocampal neuronal loss. 5 key findings →
Design: cohort study Participants: 300 Evidence: moderate
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Altogether, 187 adolescents (97 boys [51.9%]; mean age, 15.8 [0.4] years) had valid data on self-reported lifestyle behaviors, and 170 adolescents had valid data on device-assessed lifestyle behaviors. 5 key findings →
Design: cohort study Evidence: moderate
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The highest-risk group (Q4) shows a 2.8-fold increased risk of Alzheimer’s disease, a 6.4-fold risk of multiple sclerosis, and a 2.4-fold higher mortality risk. 5 key findings →
Design: cohort study Participants: 38,967 Evidence: moderate
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Per 1-m/s increase in ePWV was associated with an adjusted hazard ratio (HR) (95% confidence interval [CI]) of 1.51(1.30-1.75) for dementia and 1.58(1.33-1.89) for Alzheimer's disease (AD), and with an MMSE score decline (adjusted β-coefficient = -0.36; 95% CI = -0.52 to -0.21). 5 key findings →
Design: longitudinal study Participants: 1,857 Evidence: moderate
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Of the 2,183 participants (mean ± SD age 79 ± 4.5 years, 58% female, 24% Black), 176 (8%) developed dementia. 5 key findings →
Design: cohort study Participants: 2,183 Evidence: moderate
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During a median follow-up of 7.98 years, 896 incident dementia cases were identified among study participants. 5 key findings →
Design: prospective cohort Participants: 31,587 Evidence: moderate
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Higher cognitive reserve was associated with better cognition, fewer functional difficulties, more physical activity and better quality of life at baseline but was associated with accelerated cognitive decline and greater dependence over time. 4 key findings →
Design: longitudinal study Participants: 1,537 Evidence: moderate
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Median follow-up was 7.5 years (interquartile range: 7.0 to 9.0 years), during this time 387 participants (0.8 %) were diagnosed with dementia. 5 key findings →
Design: cohort study Participants: 47,371 Evidence: moderate
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This study included 10 333 FHS 5 key findings →
Design: cohort study Participants: 886 Evidence: moderate
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In multi-adjusted models, higher adherence to the EAT-Lancet diet was associated with higher total mean cortical thickness, and thicker cortex in Alzheimer's disease-signature regions, while a higher adherence to the MeDi was associated with better cognitive performance. 5 key findings →
Design: cohort study Participants: 615 Evidence: moderate
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Our sample included 11,105 patients (median age 77, 51% female), with 2299 in the hallway group and 8806 in the non-hallway group. 5 key findings →
Design: retrospective cohort Participants: 11,105 Evidence: moderate
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Of 689 participants, CI was associated with delirium (adjusted odds ratio [aOR]: 3.64, 95% CI: 1.31, 9.49, P-value = 0.009), 90-day complications (aOR: 2.26, 95% CI: 1.14, 4.28, P-value = 0.015), and 90-day composite adverse outcomes (aOR: 2.03, 95% CI: 1.03, 3.81, P-value = 0.033). 5 key findings →
Design: cohort study Participants: 689 Evidence: moderate
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Among 4712 participants (59% female; mean age, 74 years), 193 ischemic strokes and 769 dementia cases were ascertained over a median follow-up of 8.3 years. 5 key findings →
Design: cohort study Participants: 4,712 Evidence: moderate
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After propensity score matching, each group consisted of 15901 patients. 5 key findings →
Design: cohort study Participants: 15,901 Evidence: high
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A total of 42 342 participants from the pooled cohorts were included (mean [SD] age, 61.3 [9.8] years; 55.0% female). 5 key findings →
Design: cohort study Participants: 342 Evidence: moderate
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Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status. 5 key findings →
Design: cohort Participants: 8,582 Evidence: high
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Plasma GFAP and pTau biomarkers (pTau181, pTau231, pTau217) are significantly elevated in Aβ-positive individuals, with stronger Aβ–pTau associations observed in APOE ε4 carriers (CPAS: β = 0.26, p = 0.003 for pTau231; ADNI: β = 0.45, p < 0.001 for pTau181). 5 key findings →
Design: cohort Participants: 806 Evidence: moderate
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CSF Aβ 42 and PiB PET showed maximal correlation when collected within 6 years of each other ( R ≈ -0.5). 1 key finding →
Design: longitudinal study Participants: 371 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.
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