ADNI-3 will aim to inform AD treatment trials and facilitate development of AD disease-modifying treatments. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
ADNI-3 will aim to inform AD treatment trials and facilitate development of AD disease-modifying treatments. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by the recent identification of immune-related genetic risk factors for AD, including coding variants in the gene TREM2 (triggering receptor expressed on myeloid cells 2). 4 key findings →
Evidence: low
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Early detection of Alzheimer's disease (AD) is critical yet challenging, particularly in younger individuals. 1 key finding →
Design: longitudinal study Participants: 120 Evidence: moderate
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Plasma p‐tau217 has clinical, neuroimaging, and neuropathological correlates in sporadic FTD and may identify FTD cases with AD co‐pathology. 1 key finding →
Design: longitudinal study Participants: 620 Evidence: moderate
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Based on data from their first NACC visit with AD, there was considerable heterogeneity in language performance across people with EOAD and LOAD. 5 key findings →
Design: cross-sectional Participants: 1,189 Evidence: low
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The findings suggest that permeability of the blood-brain barrier is linked to AD pathophysiology, contributes to cerebrovascular lesions observed on MRI, and is associated with neuroinflammation in middle age. 5 key findings →
Participants: 488 Evidence: low
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We are currently in the recruitment and data collection phase. 1 key finding →
Design: cohort study Participants: 1,307 Evidence: high
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The Patient Protection and Affordable Care Act added a new Medicare benefit, the Annual Wellness Visit (AWV), effective January 1, 2011. 5 key findings →
Evidence: low
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Identifying clinical measures that track disease in the earliest stages of frontotemporal lobar degeneration (FTLD) is important for clinical trials. 4 key findings →
Participants: 31 Evidence: low
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A total of 322 participants with p-tau217, GFAP, and NfL analyses were stratified into the EOAD or FTD group based on their diagnosis. 5 key findings →
Design: cohort study Participants: 245 Evidence: moderate
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In this cohort of 2022 insulin-treated older adults with diabetes and ADRD (1011 CGM users and 1011 SMBG users; mean [SD] age, 76.4 [6.7] years; 1133 female [56.0%]), CGM use was significantly associated with lower risk of all-cause hospitalization (hazard ratio [HR], 0.86; 95% CI, 0.76-0.96) and mortality (HR, 0.57; 95% CI, 0.48-0.67) compared with SMBG use. 5 key findings →
Design: cohort study Evidence: moderate
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An important goal of advance care planning (ACP) is ensuring that patients receive care concordant with their preferences. 5 key findings →
Design: randomized controlled trial Evidence: high
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles.
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Amyloid burden is an important prognostic marker in a clinically heterogeneous cohort. 5 key findings →
Evidence: moderate
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Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci. 3 key findings →
Evidence: low
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The reasons for these differences remain unclear. 1 key finding →
Design: longitudinal study Evidence: moderate
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This study is the first clinical trial to examine the efficacy of combined physical and cognitive exercise on cognitive function in older ICU survivors with delirium. 1 key finding →
Design: randomized controlled trial Evidence: high
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Both FC-BAG and S-BAG are elevated in CI participants. 5 key findings →
Evidence: low
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The identification of mutations in the Tau gene in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) has made it possible to express human tau protein with pathogenic mutations in transgenic animals. 5 key findings →
Evidence: low
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Higher soluble plasma p-tau levels may be the result of an intersection between insoluble deposits of amyloid-β and tau accumulation in brain, and may be associated with locus coeruleus degeneration. 3 key findings →
Participants: 35 Evidence: low
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The R47H variant of Triggering Receptor Expressed on Myeloid cells 2 (TREM2) confers greatly increased risk for Alzheimer's disease (AD), reflective of a central role for myeloid cells in neurodegeneration. 4 key findings →
Evidence: low
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TabCAT tests showed good convergent validity with traditional pen-and-paper tests. 5 key findings →
Design: longitudinal study Participants: 146 Evidence: moderate
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Florbetaben PET shows high sensitivity and specificity for the detection of histopathology-confirmed neuritic β-amyloid plaques and may thus be a valuable adjunct to clinical diagnosis, particularly for the exclusion of AD.
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Defining a signature of cortical regions of interest preferentially affected by Alzheimer disease (AD) pathology may offer improved sensitivity to early AD compared to hippocampal volume or mesial temporal lobe alone. 3 key findings →
Participants: 588 Evidence: moderate
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We have used a translational convergent functional genomics (CFG) approach to identify and prioritize genes involved in schizophrenia, by gene-level integration of genome-wide association study data with other genetic and gene expression studies in humans and animal models. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 (3.7% 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 →