28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The AD subjects showed positive correlations between CSF-T-tau and CSF-P-tau versus CSF-Mn (r(s) = 0.22, p = 0.004; r(s) = 0.18, p = 0.021). 4 key findings →
Participants: 264 Evidence: low
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Mild cognitive impairment (MCI) is regarded as the prodromal stage of dementia disorders, such as Alzheimer's disease (AD). 4 key findings →
Participants: 73 Evidence: low
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A reduction of retinal thickness and an alteration of retinal perfusion have been found in Alzheimer disease (AD). 4 key findings →
Evidence: low
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Among people with multiple sclerosis, cognitive impairment occurs commonly and is a potent predictor of disability. 4 key findings →
Evidence: moderate
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Neurofilament light chain (NfL) conventionally reflects disability worsening in multiple sclerosis (MS), but does not necessarily imply MS-specific mechanisms and could be affected by biological or pathological aging, including Alzheimer disease (AD) pathology. 4 key findings →
Participants: 83 Evidence: low
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The objective was to compare the effect of HIV-1C and HIV-1B subtypes on neurofilament light (NfL) cerebrospinal fluid (CSF) levels and ratios of NfL to tau proteins. 4 key findings →
Participants: 68 Evidence: low
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Alzheimer's disease (AD) may present with pure (typical or atypical) and mixed phenotypes, sometimes causing difficulties in (differential) diagnosis. 4 key findings →
Participants: 61 Evidence: low
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It has been reported that the risk of Alzheimer's disease (AD) could be predicted by the Australian National University Alzheimer Disease Risk Index (ANU-ADRI) scores. 4 key findings →
Participants: 476 Evidence: low
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Higher serum GFAP, YKL-40, sCD14, and NfL were associat 4 key findings →
Participants: 3,082 Evidence: low
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Blood-based biomarkers are increasingly used to characterize Alzheimer's disease (AD)-related pathology, yet substantial heterogeneity exists in how biomarker burden relates to cognitive performance. 4 key findings →
Design: cross-sectional Participants: 348 Evidence: low
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We found 5 distinct clusters of subjects (N=38, N=16, N=24, N=14, N=21) with a composition statistically independent from that obtained using available clinical diagnostic criteria (each cluster included all phenotypical groups). 3 key findings →
Participants: 20 Evidence: moderate
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Among CU participants, men had lower Aβ42 and GFAP, and higher p-tau217/Aβ42. 5 key findings →
Evidence: low
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Plasma biomarkers demonstrate promise for improving diagnostic accuracy in diverse research cohorts. 3 key findings →
Evidence: moderate
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Vascular burden influences NfL levels, particularly in A- individuals at a symptomatic stage. 5 key findings →
Design: cross-sectional Participants: 421 Evidence: moderate
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The dominant research paradigm for Alzheimer's disease has focused on amyloid-beta plaqueremoval for over three decades, producing no curative therapy despite billions of dollars ofinvestment. 2 key findings →
Evidence: low
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We observed differential cellular effects on β-amyloid, pTau217 and cognitive measures. 3 key findings →
Participants: 734 Evidence: moderate
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Our results emphasize the role of fluid biomarkers in diagnosing dementia in low‐resource settings in South Asians. 5 key findings →
Participants: 70 Evidence: moderate
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In both cohorts there were significant associations between CSF MTBR-tau243 and the temporal meta-ROI (BioFINDER-2: t = 17.1, p < 0.001, Knight-ADRC: t=11.0, p <0.001). 5 key findings →
Design: cross-sectional Evidence: moderate
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A total of 51 patients with AD, age (median: 73 years) and 53 cognitively normal subjects (median age: 69) were included. 5 key findings →
Participants: 51 Evidence: low
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Blood-based biomarkers hold significant promise for the early detection and diagnosis of Alzheimer’s disease (AD) and other dementias. 5 key findings →
Evidence: low
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MAP-RTAP (AUC = 0.78) and pTau/Aβ42 (AUC = 0.76) were the best performing individual biomarkers. 4 key findings →
Evidence: low
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There are increasing calls for sharing individual biomarker results with participants in dementia research. 5 key findings →
Evidence: low
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The STUB1/CHIP holds promise as a potential biomarker for distinguishing between SCI subjects, AD, and FTD. 5 key findings →
Participants: 90 Evidence: low
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Vascular dementia (VaD) is the second most common cause of dementia. 2 key findings →
Evidence: low
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CSF BD‐tau shows potential as a biomarker of treatment effect in AD but not bvFTD. 1 key finding →
Evidence: moderate
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10 of the 3,322 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →