28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In this case-control study, blood biomarkers indicative of AD pathology demonstrated different dynamics of change after cardiac arrest. 5 key findings →
Design: case-control study Participants: 80 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This Swedish study of over 1,200 people with memory symptoms found that a blood test combining p-tau217 with an amyloid ratio (the 'Amyloid Probability Score 2') was far more accurate at identifying Alzheimer's disease than doctors' clinical judgment alone. 3 key findings →
Design: cross-sectional Participants: 1,213 Evidence: high
Full summary, score breakdown and related studies → Original source
We found low intra-individual variability, robust to various factors, appropriate to capture individual changes in AD BBMs, while moderate inter-individual variability may give rise to caution in diagnostic contexts. 2 key findings →
Design: longitudinal study Participants: 27 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau biomarkers had a greater diagnostic performance and larger effect sizes compared to t-tau and Aβ42/40 assays in detecting Aβ pathology. 5 key findings →
Design: cross-sectional Participants: 197 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher levels of P-tau181 (HR = 1.32 [95% CI: 1.17-1.51]), NfL (HR = 1.19 [95% CI: 1.03-1.36]), and GFAP (HR = 1.36 [95% CI: 1.22-1.52]), and a lower Aβ42/Aβ40 ratio (HR = 0.80 [95% CI: 0.68-0.95]) were associated with an increased risk of progressing to clinically-diagnosed DAT. 2 key findings →
Design: longitudinal study Participants: 1,007 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217 and p-tau217/Aβ42 concentrations demonstrated robust diagnostic performance in a heterogeneous clinical cohort; interpretation requires consideration of kidney function. 5 key findings →
Design: cross-sectional Participants: 509 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Several plasma p-tau biomarkers can be used in a specialized memory clinic as a stand-alone biomarker to detect biologically-defined AD. 2 key findings →
Participants: 197 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers for screening may guide tau positrion emissition tomography (PET) scan referrals to optimize prognostic evaluation in Alzheimer's disease. 2 key findings →
Participants: 548 Evidence: low
Full summary, score breakdown and related studies → Original source
Performance was assessed in comparison to clinical diagnosis (blinded to plasma results) and amyloid status (CSF/PET). 4 key findings →
Participants: 268 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma tau phosphorylated at threonine 181 (p-tau181) and 217 (p-tau217) have demonstrated high accuracy for Alzheimer's disease (AD) diagnosis, defined by CSF/PET amyloid beta (Aβ) positivity, but most studies have been performed in research cohorts, limiting their generalizability. 3 key findings →
Participants: 468 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 demonstrated better performance in the identification of AD pathology and clinical phenotypes in comparison with other variants of p-tau in a memory clinic cohort. 5 key findings →
Participants: 114 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by brain protein depositions, impaired synaptic transmission, and progressive cognitive decline. 2 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative biomarkers were elevated to levels observed in AD dementia and associated with encephalopathy and worse outcomes among hospitalized COVID-19 patients. 5 key findings →
Participants: 251 Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to Simoa biomarkers, APEX-Aβ42 showed significantly higher correlations with amyloid PET retention values and excellent diagnostic performance (sensitivity 100%, specificity 93.3%, area under the curve 0.995). 4 key findings →
Participants: 68 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
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
CSF Aβ42/40 ratio can predict PET amyloid positivity with high accuracy in patients with a range of cognitive disorders when evaluating Aβ pathology independent of tau and neurodegeneration for research purposes. 4 key findings →
Participants: 44 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma biomarkers have shown promising performance in research cohorts in discriminating between different stages of Alzheimer's disease (AD). 2 key findings →
Participants: 75 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although plasma pTau181, pTau217, pTau231, and GFAP were significantly associated with both Aβ-PET and CSF pTau181, Aβ-PET explained more variance in the levels of these biomarkers. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The proteomic profile discriminated DLB and PD from NC with an AUC (Area Under the Curve) of 0.96 with demographics of age, sex and education. 4 key findings →
Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source
Vitamin D deficiency was common among nursing home residents and strongly associated with dementia. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
SNfL was perceived as useful in 53% (n = 58) of the cases. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Closing this gap will require the introduction of high-performing blood tests, greater reliance on cerebrospinal fluid (CSF) testing, and expansion of positron emission tomography (PET) capacity. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular burden influences NfL levels, particularly in A- individuals at a symptomatic stage. 5 key findings →
Design: cross-sectional Participants: 421 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Vascular burden influences NfL levels, particularly in amyloid‐negative individuals. 5 key findings →
Participants: 371 Evidence: moderate
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 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 →