27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The cross-sectional difference in 2 independent neuroimaging modalities indicates early AD pathology in SMI. 2 key findings →
Design: cross-sectional Participants: 31 Evidence: moderate
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We found no significant correlation between CSF biomarkers and cognitive scores in any of the 3 clinical groups individually. 2 key findings →
Design: cross-sectional Participants: 399 Evidence: low
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In a middle-aged, at-risk cohort, a physically active lifestyle is associated with an attenuation of the deleterious influence of age on key biomarkers of AD pathophysiology. 3 key findings →
Design: cross-sectional Participants: 186 Evidence: high
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Increased WMHs are associated with aging, decreased glucose metabolism, and decline in executive function but do not affect AD-specific pathologic progression, suggesting that the vascular contribution to dementia is probably additive although not necessarily independent of the amyloid pathway. 5 key findings →
Design: longitudinal study Evidence: moderate
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ARIA-E can also occur spontaneously in cerebral amyloid angiopathy-related inflammation (CAA-ri), a rare autoimmune encephalopathy associated with increased CSF levels of anti-Aβ autoantibodies. 5 key findings →
Design: longitudinal study Evidence: moderate
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Limiting the clinical use of definite anticholinergics may reduce the incidence of cognitive impairment among African Americans. 2 key findings →
Design: longitudinal study Evidence: moderate
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Dementia is frequent after ischemic stroke, occurring in one-fourth of the elderly patients in the authors' cohort. 3 key findings →
Participants: 453 Evidence: moderate
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Poorer OI in older adults without dementia was associated with increased risk of dementia. 5 key findings →
Participants: 2,428 Evidence: low
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The ACE is a brief and reliable bedside instrument for early detection of dementia, and offers a simple objective index to differentiate AD and FTD in mildly demented patients. 2 key findings →
Participants: 115 Evidence: low
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Women who underwent either unilateral or bilateral oophorectomy before the onset of menopause had an increased risk of cognitive impairment or dementia compared to referent women (hazard ratio [HR] = 1.46; 95% CI 1.13 to 1.90; adjusted for education, type of interview, and history of depression). 2 key findings →
Participants: 813 Evidence: moderate
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Contrary to previous reports, head trauma was not a risk factor for AD, and smoking did not protect against AD. 4 key findings →
Design: cross-sectional Evidence: moderate
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Patients with mild cognitive impairment (MCI) showed a high probability to be diagnosed with Alzheimer dementia (AD) after 30 months. 1 key finding →
Participants: 1,505 Evidence: moderate
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Having multiple CMBs or concomitant CMBs and retinopathy is associated with a profile of vascular cognitive impairment. 5 key findings →
Design: cross-sectional Participants: 3,906 Evidence: low
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The designed battery consists of six subtests exploring the following: conceptualization, mental flexibility, motor programming, sensitivity to interference, inhibitory control, and environmental autonomy. 1 key finding →
Participants: 24 Evidence: low
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There were insufficient data to make any recommendations regarding cognitive screening of asymptomatic individuals. 4 key findings →
Evidence: low
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The predictive validity of mild cognitive impairment (MCI) for identifying future Alzheimer disease (AD) cases is improved in the presence of anxiety symptoms. 1 key finding →
Participants: 185 Evidence: low
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Compare cognitive and hippocampal volume trajectories in asymptomatic middle-aged and older adults with positive CSF markers of β-amyloid (Aβ) or tau to adults without an Alzheimer disease (AD)-associated biomarker profile. 4 key findings →
Design: cohort study Participants: 78 Evidence: moderate
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The neuropathologic changes underlying Alzheimer disease (AD) start before overt cognitive symptoms arise, but it is not well-known how they relate to the first subtle cognitive changes. 4 key findings →
Design: cross-sectional Participants: 217 Evidence: moderate
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The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia. 4 key findings →
Design: longitudinal study Participants: 350 Evidence: moderate
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Treatment options for Alzheimer disease (AD) are limited and have focused mainly on symptomatic therapy and improving quality of life. 4 key findings →
Design: cross-sectional Evidence: low
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It has been suggested that the risk might be particularly increased for carriers of the APOE-epsilon4 allele. 4 key findings →
Design: cross-sectional Participants: 6,645 Evidence: moderate
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We evaluated dementia-free Framingham Heart Study (generation 3) participants (mean age 48.5 years, 46.8% men) who underwent cognitive testing for memory, abstract reasoning, visual perception, attention, and executive function (n = 2,231) and brain MRI (n = 2018) to assess total white matter, lobar gray matter, and white matter hyperintensity volumes and fractional anisotropy (FA) measures. 4 key findings →
Participants: 2,231 Evidence: low
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Analyses were performed within the Rotterdam Study (baseline 1997), a prospective, population-based cohort. 4 key findings →
Participants: 9,446 Evidence: moderate
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We aimed to investigate whether the increased risk of dementia among individuals with diabetes can be offset by a broad combination of healthy lifestyle factors. 4 key findings →
Participants: 167,946 Evidence: moderate
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Given the potential therapeutic effect of vascular disease control timing to reduce dementia risk, we investigated the age-related influences of vascular risk factor burden on brain structure throughout the lifespan. 4 key findings →
Design: cross-sectional Participants: 2,887 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 27,380 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 →