The increasing availability of single-cell data revolutionizes the understanding of biological mechanisms at cellular resolution. 4 key findings →
Evidence: moderate
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28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
The increasing availability of single-cell data revolutionizes the understanding of biological mechanisms at cellular resolution. 4 key findings →
Evidence: moderate
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A significant reduction in underdiagnosis of dementia was observed between the two periods, consistent across most countries. 4 key findings →
Participants: 10,402 Evidence: low
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Linear and logistic regression showed that childhood rural residence was associated with lower memory (standardized beta (β) = -1.68, 95% Confidence Interval (CI) [-2.39, -0.97]), executive function (β = -1.20, 95% CI [-1.84, -0.55]), and language fluency (β = -0.86, 95% CI [-1.64, -0.08]). 5 key findings →
Participants: 3,073 Evidence: low
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Hypertension, acute myocardial infarction, atrial fibrillation, diabetes, heart failure, ischemic heart disease, stroke, and arthritis additively accounted for 71.8% (95% confidence interval [CI]: 62.9%-79.1%) of ADRD incident cases based on LE-AAF. 5 key findings →
Design: longitudinal study Evidence: moderate
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This paper examines eight published reviews that each pooled results from several related clinical trials to evaluate treatment efficacy. 4 key findings →
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Caregiver characteristics and provision of caregiving tasks determine caregiver burden more than care recipient characteristics. 5 key findings →
Evidence: low
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Approximately 10% of dementia patients have idiopathic normal pressure hydrocephalus (iNPH), an expansion of the cerebrospinal fluid (CSF)-filled brain ventricles. iNPH and Alzheimer's disease (AD) both exhibit sleep disturbances, build-up of brain metabolic wastes and amyloid-β (Aβ) plaques, perivascular reactive astrogliosis, and mislocalization of astrocyte aquaporin-4 (AQP4). 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is hallmarked by amyloid plaques, neurofibrillary tangles, and widespread cortical neuronal loss (Selkoe, 2001). 4 key findings →
Evidence: low
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Currently no effective disease-modifying agents exist for the treatment of Alzheimer disease (AD). 4 key findings →
Evidence: low
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CSF sTREM2 increased with systemic and CNS HIV-1 disease severity, with the highest levels found in patients with HIV-associated dementia (HAD). 4 key findings →
Design: cross-sectional Evidence: low
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Patients with CLTI undergoing peripheral vascular intervention from 2017 to 2018 were derived from the Medicare-linked VQI (Vascular Quality Initiative) registry. 5 key findings →
Participants: 114 Evidence: moderate
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In the ADMET2 biomarker subset (n = 44, MPH:21, age:75 years, MMSE:20.2), higher baseline TNF was associated with higher M6 NPI-A [B(SE)= 6.86 (1.71), p = .0003], and multivariable models found lower baseline TNF [B(SE)= 8.28(1.61), p < .001] and higher baseline S100B [B(SE)= -6.41(1.95), p = .002] were associated with lower M6 NPI-A. Exploratory analyses suggested that higher baseline NfL significantly interacted with treatment to predict lower M6 NPI-A [B(SE)= -8.36(4.21), p = .05], only when adjusting for cognition. 5 key findings →
Participants: 44 Evidence: high
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The CAM is sensitive, specific, reliable, and easy to use for identification of delirium.
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Physostigmine demonstrated a statistically significant benefit compared with placebo on a clinical global rating of change and an objective test of cognitive function. 3 key findings →
Participants: 850 Evidence: high
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Warfarin anticoagulation with atrial fibrillation, even among "ideal" candidates, appears dramatically underutilized. 2 key findings →
Participants: 488 Evidence: low
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A significant ADI × dementia interaction was observed for global atrophy (p = .005) and several other outcomes. 5 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
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Vestibular disorders were linked to higher risks of all‐cause dementia (HR 1.86 and 95% CI 1.04–3.30), Alzheimer's disease (AD, 2.36, and 1.01–5.51), and vascular dementia (VD, 3.35, and 1.48–7.59). 5 key findings →
Design: cohort study Evidence: moderate
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Despite the success of large-scale genome-wide association studies (GWASs) on complex traits, our understanding of their genetic architecture is far from complete. 2 key findings →
Evidence: low
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Among mild to moderate AD patients, enrolled in an actual clinical trial, these results suggest evidence based guidelines for using the MacCAT-CR understanding subscale to help guide judgments about whether a patient has the capacity to consent. 3 key findings →
Design: cross-sectional Evidence: high
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This study examined the validity of the four standard psychological paradigms that have been operationally defined within the CogState brief computerized cognitive assessment battery. 1 key finding →
Evidence: low
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A chart-based instrument for delirium, which should be useful for patient safety and quality-improvement programs in older persons, was validated. 5 key findings →
Evidence: low
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Most older patients surviving AMI have measurable CIND. 2 key findings →
Participants: 772 Evidence: low
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We present a multivariate alternative to the voxel-based morphometry (VBM) approach called source-based morphometry (SBM), to study gray matter differences between patients and healthy controls. 4 key findings →
Evidence: low
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Neuropathology involving TAR DNA binding protein-43 (TDP-43) has been identified in a wide spectrum of neurodegenerative diseases collectively named as TDP-43 proteinopathy, including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar dementia (FTLD). 4 key findings →
Evidence: low
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Mitochondrial aldehyde dehydrogenase (ALDH2) is one of the most important enzymes in human alcohol metabolism. 4 key findings →
Participants: 4,091 Evidence: low
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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 →