28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebrospinal fluid (CSF) neurofilament light (NFL) is a marker of axonal degeneration. 2 key findings →
Design: longitudinal study Participants: 144 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers of AD/ADRD are influenced by common demographic and clinical characteristics. 2 key findings →
Participants: 779 Evidence: high
Full summary, score breakdown and related studies → Original source
After adjusting for age, sex, and the apolipoprotein E ( APOE ) alleles, compared to the CN group, the plasma t-tau, and NfL were significantly increased in the AD group ( p < 0.01, Bonferroni correction). 4 key findings →
Design: cross-sectional Participants: 277 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results show that the measurement of p-Tau181 in plasma has great potential as a non-invasive prognostic screening tool for implementation in a clinical setting. 5 key findings →
Participants: 138 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings indicate that the high plasma AβO level could serve as a potential surrogate biomarker of severe SCD and the presence of brain Aβ deposition in individuals with normal objective cognition. 5 key findings →
Design: cross-sectional Participants: 126 Evidence: low
Full summary, score breakdown and related studies → Original source
Early diagnosis of Alzheimer's disease (AD) is a crucial starting point in disease management. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Researchers at the University of Pittsburgh developed a new plasma p-tau217 test (using a different antibody than existing commercial tests) and validated it in 363 people, including some with genetic early-onset Alzheimer's mutations and community-dwelling older adults. 4 key findings →
Design: cross-sectional Participants: 363 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF biomarkers, including P-tau, T-tau, Aβ 42 , Aβ 40 , and NFL, support in vivo identification of AD neuropathology and correlate with FTLD neuropathology. 4 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The combination of sAPPβ with YKL-40 and with NfL in CSF could be useful to increase the certainty of the diagnosis of FTLD-related syndromes in clinical practice. 2 key findings →
Design: cross-sectional Participants: 159 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Although all p-tau variants increased across the AD continuum, p-tau217 Lilly showed the greatest dynamic range (13-fold increase vs 1.9-5.4-fold increase for other p-tau variants for AD dementia vs non-AD). 2 key findings →
Participants: 334 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid positron emission tomography (PET) imaging is being investigated as a screening tool to identify amyloid-positive patients as an enrichment strategy for Alzheimer disease (AD) clinical trial enrollment. 1 key finding →
Participants: 278 Evidence: low
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We developed, replicated, and validated an MRI measure of cerebrovascular and neurodegenerative pathologies that are associated with clinical and neuropathologic diagnosis of AD and related to established biomarkers. 5 key findings →
Design: cross-sectional Participants: 1,175 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In methodologically heterogeneous studies of uncertain applicability to typical clinical settings, amyloid PET, 18 F-FDG PET, and MRI were highly sensitive for neuropathologic AD. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
= 0.02, 95% CI -0.07 to -0.01) network connectivity. 5 key findings →
Design: longitudinal study Participants: 421 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 621 participants (aged 69.9 ± 3.8, 71% female) had available data for the main analyses and 355 had PET Centiloid data available. 5 key findings →
Design: cross-sectional Participants: 621 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A total of 365 participants (mean [SD] age, 75.4 [7.9] years; 192 female [52.6%]) in the ADNI tau-PET group and 524 participants (mean [SD] age, 77.1 [7.9] years; 268 male [51.1%]) in the ADNI p-tau217 group were selected from the 998 individuals who were Aβ+ in the ADNI cohort and used to generate tau-clinical mismatch models with 55.6% to 57.1% classified as canonical (CDR-SB commensurate to tau), 23.7% to 24.7% as resilient (CDR-SB tau). 5 key findings →
Design: cohort study Participants: 365 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Blood phosphorylated (p)-tau 181 and p-tau 217 have been proposed as accurate biomarkers of Alzheimer's disease (AD) pathology. 2 key findings →
Participants: 152 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated-tau217 (p-tau217) has been shown to be one of the most accurate diagnostic markers for Alzheimer's disease. 3 key findings →
Participants: 392 Evidence: low
Full summary, score breakdown and related studies → Original source
To improve clinical utility, a dual threshold approach was applied to maximize predictive values and positive likelihood ratios while minimizing the proportion of indeterminate results. 5 key findings →
Participants: 208 Evidence: low
Full summary, score breakdown and related studies → Original source
Among 191 participants (57 Black, 46 Hispanic White, 88 non-Hispanic White), age-adjusted plasma p-tau217 and p-tau217/Aβ42 performed similarly in detecting amyloid-positive individuals (≥ 25 Centiloids), regardless of race/ethnicity. 5 key findings →
Participants: 191 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 demonstrated the strongest discrimination of Core1 positivity (area under the curve [AUC] = 0.95) and showed the steepest increase with disease progression. 4 key findings →
Participants: 401 Evidence: low
Full summary, score breakdown and related studies → Original source
Greater MVPA (β = -0.107; p = 0.013) and CRF (β = -0.114; p = 0.027) were associated with lower NfL, but not Aβ PET, p-tau217, Aβ1-42/1-40, or GFAP. 4 key findings →
Participants: 648 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid status was determined by CSF in 347 patients (189 positive [54.5%]) and by PET imaging in 152 patients (66 positive [43.4%]). 4 key findings →
Participants: 499 Evidence: low
Full summary, score breakdown and related studies → Original source
Aβ-independent factors included hemoglobin and estimated glomerular filtration rate (eGFR) for p-tau217 and hemoglobin, eGFR, and triiodothyronine (T3) for GFAP and NfL. 5 key findings →
Participants: 2,935 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 →