Of 2,218 participants, 237 (11%) developed dementia in the period 1992/3 to 2015/6. 5 key findings →
Design: cohort study Participants: 2,218 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 2,218 participants, 237 (11%) developed dementia in the period 1992/3 to 2015/6. 5 key findings →
Design: cohort study Participants: 2,218 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Anxiety, apathy and depression are common in subjects with mild cognitive impairment (MCI) and may herald Alzheimer's disease (AD). 4 key findings →
Participants: 268 Evidence: low
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We increased the findability, accessibility, interoperability and reusability (FAIR) status of the cohorts through harmonization of data across cohorts, implementation of medical imaging repositories for scan management, implementation of the Personal Health Train infrastructure and provision of meta-data in existing cohort catalogues. 5 key findings →
Design: meta-analysis Evidence: high
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Between 1997 and 2016, we repeatedly assessed cognitive function with 5 tests in 9514 participants aged 45-90 years from the population-based Rotterdam Study. 4 key findings →
Participants: 9,514 Evidence: low
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We included 17098 records, 4139 from deceased individuals (mean age 81) and 12959 from living individuals (mean age 79). 4 key findings →
Design: case-control study Participants: 17,098 Evidence: moderate
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Cohort 1 included 446 individuals (mean age (SD) 65.2 years (8.9); 203 women), Cohort 2 included 164 individuals (mean age (SD) 49.9 years (12.6); 88 women). 5 key findings →
Design: longitudinal study Participants: 446 Evidence: moderate
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The results of this proof-of-principle study will be used to assess the potential of target engagement of minocycline for CAA. 1 key finding →
Participants: 60 Evidence: high
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[(11)C]PIB scans were positive in 40 of 66 (61%) patients with a clinical diagnosis of Alzheimer's disease (AD), 5 of 18 (28%) patients with frontotemporal dementia (FTD), 4 of 5 (80%) patients with Lewy body dementia, and 3 of 10 (30%) patients with other dementias. [(18)F]FDG uptake patterns matched the clinical diagnosis in 38 of 66 (58%) of AD patients, and in 6 of 18 (33%) FTD patients. 4 key findings →
Participants: 39 Evidence: low
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Participants included 202 physicians and three nurse specialists who assumed similar medical responsibilities. 5 key findings →
Design: cross-sectional Participants: 202 Evidence: low
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Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia with no specific treatment, of which molecular mechanisms remain poorly understood. 2 key findings →
Participants: 40,000 Evidence: low
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Cerebral amyloid angiopathy is caused by deposition of the amyloid beta protein in the cerebral vasculature. 4 key findings →
Evidence: low
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Plasma amyloid-β (Aβ) levels are increasingly studied as a potential accessible marker of cognitive impairment and dementia. 4 key findings →
Participants: 458 Evidence: low
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Being overweight or obese, as measured with body-mass index or central adiposity (waist circumference), and the trajectory of body-mass index over the life course have been associated with brain atrophy, white matter changes, disturbances of blood-brain barrier integrity, and risk of all-cause late-onset dementia and Alzheimer's disease. 4 key findings →
Evidence: low
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• Longitudinal imaging-genetics study of hippocampal atrophy trajectories over 5 years in ADNI. • APOE -ε4 carriership and ApoE CSF proteomic quantitative trait loci are key genetic drivers of accelerated hippocampal atrophy in amyloid-positive MCI. • Genetic effects are stage-specific, with strongest associations during the prodromal phase of AD. • Sex differences in atrophy rates are observed, but do not significantly alter genetic influences. • Findings support the utility of APOE and functional genetic markers as stratification tools for early neurodegeneration in AD. 4 key findings →
Design: longitudinal study Participants: 1,051 Evidence: moderate
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A total of 44 experts participated in 3 survey rounds, with 28 to 31 participants each. 5 key findings →
Participants: 31 Evidence: low
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Statistical interdependencies between magnetoencephalographic signals recorded over different brain regions may reflect the functional connectivity of the resting-state networks. 5 key findings →
Evidence: low
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This study provides evidence for heterogeneous pathologic substrates and possibly different pathophysiologic mechanisms underlying MRI-observed cortical microbleeds in the context of advanced CAA and Alzheimer disease. 1 key finding →
Evidence: low
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In adjusted analyses, the rate of first ACP conversation for persons with organ failure was the lowest (IRR 0.70 (95% CI 0.68 to 0.73)). 5 key findings →
Design: longitudinal study Evidence: moderate
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Dementia is a clinical diagnosis without curative treatment. 3 key findings →
Design: cohort study Participants: 13,312 Evidence: moderate
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Cerebrovascular disease (CVD) and amyloid-β (Aβ) often coexist, but their influence on neurodegeneration and cognition in predementia stages remains unclear. 4 key findings →
Participants: 99 Evidence: moderate
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The occurrence of obesity, commonly estimated using body mass index (BMI), and the most common late-onset dementia, Alzheimer's disease (AD), are increasing globally. 4 key findings →
Evidence: low
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Thirty constitutive elements of ACP were identified (e.g., 'assess understanding of ACP'). 5 key findings →
Evidence: low
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The DEDICATED approach was implemented across 28 wards in three healthcare organizations. 5 key findings →
Design: longitudinal study Participants: 17 Evidence: moderate
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This manuscript is the second part of a two-part description of the current status of understanding of the network function of the brain in health and disease. 5 key findings →
Evidence: low
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This work was supported by a Crossover grant (Maintaining Optimal Cognitive Functioning In Aging [MOCIA] 17611) of the Dutch Research Council (NWO), granted in December 2019. 5 key findings →
Participants: 102 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →