27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In this prospective cohort study, higher consumption of UPF was associated with higher risk of dementia, whereas substituting unprocessed or minimally processed foods for UPF was associated with lower risk of dementia. 5 key findings →
Design: cohort Participants: 72,083 Evidence: moderate
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In this nationwide population-based study, SGLT2i use significantly reduced the risks of neurodegenerative disorders in patients with type 2 diabetes independent of various factors including comorbidities and bioclinical parameters. 5 key findings →
Design: cohort Participants: 358,862 Evidence: moderate
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Overall, 2,277 individuals had at least 1 baseline blood biomarker available (n = 357 for CSF subsample, n = 649 for PET subsample), among whom 257 were diagnosed with clinical AD/mixed dementia during follow-up. 2 key findings →
Design: prospective cohort Participants: 357 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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In DDI (n = 431), participants were classified as CN A-/T- (n = 169), A+/T- (CN = 26, MCI = 24), A+/T+ (CN = 40, MCI = 105), and A-/T+ (CN = 34, MCI = 33), with a mean age of 64.1 years and 55.9% female. 2 key findings →
Design: longitudinal study Participants: 431 Evidence: moderate
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Over 10 years of close clinical dementia surveillance in this cohort study, loneliness was associated with increased dementia risk; this tripled in adults whose baseline risk would otherwise be relatively low on the basis of age and genetic risk, representing a majority of the US population. 5 key findings →
Design: cohort study Participants: 2,308 Evidence: moderate
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Increased levels of triglycerides at midlife predict brain Aβ and tau pathology 20 years later in cognitively healthy individuals. 5 key findings →
Design: cohort study Participants: 134 Evidence: moderate
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Quetiapine was well-tolerated and did not worsen parkinsonism. 3 key findings →
Participants: 23 Evidence: high
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High cholesterol in late life was associated with decreased dementia risk, which is in contrast to previous studies suggesting high cholesterol in mid-life is a risk factor for later dementia. 5 key findings →
Design: longitudinal study Participants: 392 Evidence: moderate
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APOE ε4 may influence the association between WMH and cognitive performance in AD and DLB. 5 key findings →
Design: meta-analysis Participants: 167 Evidence: high
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The highly consistent regional hierarchy of PET-evidenced amyloid deposition across participants resembles neuropathologic observations and suggests a predictable regional sequence that may be used to stage an individual's progress of amyloid pathology in vivo. 2 key findings →
Design: cross-sectional Participants: 667 Evidence: moderate
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Low-dose risperidone (mean 1.1 mg/d) was well tolerated and associated with reductions in the severity and frequency of behavioral symptoms, particularly aggression, in elderly patients with dementia. 5 key findings →
Participants: 344 Evidence: low
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In this population, among those who progressed to dementia, 60% progressed to AD and 33% to VaD. 2 key findings →
Design: longitudinal study Participants: 2,963 Evidence: moderate
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Our findings support the hypothesis that depression is a risk factor for dementia and suggest that recurrent depression is particularly pernicious. 3 key findings →
Design: longitudinal study Participants: 1,239 Evidence: moderate
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Early identification of patterns of abnormality is of fundamental importance for detecting disease onset and tracking progression. 2 key findings →
Design: longitudinal study Participants: 1,017 Evidence: moderate
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DNA methylation algorithms are increasingly used to estimate biological aging; however, how these proposed measures of whole-organism biological aging relate to aging in the brain is not known. 4 key findings →
Design: longitudinal study Participants: 649 Evidence: moderate
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We tested the hypothesis that cerebral amyloid angiopathy (CAA) is related to Alzheimer disease (AD) dementia and decline in multiple cognitive systems in old age, independent of AD plaque and tangle pathology and other common age-related neuropathologies. 4 key findings →
Design: longitudinal study Participants: 1,113 Evidence: moderate
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The incidence of MCR is high in older adults. 2 key findings →
Design: cohort study Participants: 3,128 Evidence: moderate
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We included 401 individuals (61±9 years, 42% female, MMSE 28 ± 2, vascular comorbidities 8%-19%). 5 key findings →
Design: cohort study Participants: 401 Evidence: moderate
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The overall frequency of LATE-NC in Black and White decedents was similar (40.8% vs 45.4%). 5 key findings →
Design: longitudinal study Participants: 76 Evidence: moderate
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CKD was associated with increased p-tau217 concentrations when measuring p-tau217 by ALZpath and C 2 N methodologies, but the effect was mitigated by the use of %p-tau217. 5 key findings →
Design: cross-sectional Participants: 202 Evidence: moderate
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Progression from amnestic mild cognitive impairment to Alzheimer disease in this cohort was best determined by combining four common, easily administered, cognitive measures. 1 key finding →
Participants: 539 Evidence: moderate
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The findings of the current study show that the longitudinal, cumulative trajectory of cardiovascular risk is predictive of dementia risk and associated with the emergence of memory decline. 4 key findings →
Design: prospective cohort Participants: 1,244 Evidence: moderate
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Primary clinical efficacy outcomes were not significant. 5 key findings →
Design: clinical trial Participants: 84 Evidence: high
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PF-04494700 at 20 mg/d was associated with increased adverse events and cognitive decline. 3 key findings →
Participants: 399 Evidence: high
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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 →