27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma p-tau181 had correlations with broader cognitive domains, suggesting its potential as a promising clinical-relevant blood-based biomarker. 2 key findings →
Participants: 320 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Lumipulse G assays show a very good analytical performance that makes them well-suited for CSF clinical routine measurements. 4 key findings →
Participants: 80 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Dominantly Inherited Alzheimer Network (DIAN) is an international registry of individuals at risk for developing autosomal dominant Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
When benchmarked against amyloid PET, plasma biomarker-based stratification achieves an optimal balance between diagnostic accuracy and cost-effectiveness. 5 key findings →
Participants: 143 Evidence: low
Full summary, score breakdown and related studies → Original source
The PRS using 131 SNPs had an effect independent of APOE. 5 key findings →
Participants: 565 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hyperspectral data and retinal nerve fiber layer thickness data were used in a linear discriminant classification model to discriminate between AD patients and controls. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Ninety-four proteins differentiated in the high-risk group compared to low-risk (p < 0.05), none surviving FDR correction. 5 key findings →
Participants: 156 Evidence: moderate
Full summary, score breakdown and related studies → Original source
While the field advances towards consensus definitions of existing concepts, the resistance vs resilience terminology may provide clarity in the communication of results in aging and dementia studies as well as provide a framework for the development of both hypotheses and study designs. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified 59 key microbial species linked to MCI and AD biomarkers. 5 key findings →
Participants: 119 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) neuropathology is associated with neuroinflammation, but there are few useful biomarkers. 4 key findings →
Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Altered proteome profiles have been reported in both postmortem brain tissues and body fluids of subjects with Alzheimer disease (AD), but their broad relationships with AD pathology, amyloid pathology, and tau-related neurodegeneration have not yet been fully explored. 4 key findings →
Design: cross-sectional Participants: 48 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Despite significant progress, a disease-modifying therapy for Alzheimer's disease (AD) has not yet been developed. 4 key findings →
Participants: 24 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Recent studies suggest that plasma phosphorylated tau181 (p-tau181) is a highly specific biomarker for Alzheimer's disease (AD)-related tau pathology. 4 key findings →
Participants: 818 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to identify lipid species associated with MPH response and explore lipid pathway disruptions in responders versus non-responders. 3 key findings →
Design: randomized controlled trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Sixty-nine HC, 13 preclinical AD, 38 AD-MCI, 44 AD-D, and 79 non-AD CI participants were included. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ- groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). 5 key findings →
Participants: 212 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Lower CSF Amyloid beta 1-42 concentrations (p = 0.048), lower Amyloid beta 42/40 ratio (p = 0.038), and higher Tau/Amyloid-beta 1-42 ratio, as well as pTau/Amyloid-beta 1-42 ratio (each p = 0.004) were associated with rpAD. 5 key findings →
Participants: 228 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In response to correspondence from Cognivue, Inc. regarding our publication (Jannati et al., 2025), we clarify that our analysis employed a rigorous paired-sample design using the same 930 participants from the Bio-Hermes-001 study for both the Digital Clock and Recall® (DCR) and Cognivue Clarity® assessments. 3 key findings →
Participants: 930 Evidence: low
Full summary, score breakdown and related studies → Original source
Differential FTP-PET signal patterns showed significant negative associations with domain-specific annual rates of decline. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
The SVCI group showed lower CD in the temporal quadrant of the RPC network compared to the CN group (mean (SD), 42.34 (6.29) vs 48.45 (7.08); p = 0.001). 5 key findings →
Design: cross-sectional Participants: 69 Evidence: low
Full summary, score breakdown and related studies → Original source
CR varied across five cognitive assessments and was greater in female participants, associated with longer survival, and weakly associated with educational attainment or APOE ε4 allele. 5 key findings →
Participants: 844 Evidence: moderate
Full summary, score breakdown and related studies → Original source
MR analysis suggested a causal relationship between decreased blood-derived mtDNA-CN and increased risk of AD (OR = 0.68; P = 0.013). 5 key findings →
Participants: 13,799 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of 108 participants (age: 69 ± 6.5 years; 54.6% female) with paired samples obtained at time of LP, 64.8% (n = 70/108) had Aβ pathology detected (35 with Mild Cognitive Impairment and 35 with mild dementia). 2 key findings →
Participants: 70 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Due to the progressive aging of the population, Alzheimer's disease (AD) is becoming a healthcare burden of epidemic proportions for which there is currently no cure. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that the loss of perivascular AQP4 localization may contribute to the development of AD pathology in human populations. 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 27,380 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 →