30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The double-cutoff approach revealed high confidence for interpreting scans as negative when Centiloid values were lower than 11 (95% CI, 9-13; I2 = 95%) and interpreting scans as positive if Centiloid values were higher than 26 (95% CI, 24-28; I2 = 95%). 3 key findings →
Design: meta-analysis Participants: 49,227 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Between May 18, 2021, and Sept 8, 2023, 9981 participants were screened, of whom 3808 were randomly assigned; 1855 in evoke (semaglutide, n=928; placebo, n=927) and 1953 in evoke+ (semaglutide, n=976; placebo, n=977). 5 key findings →
Design: clinical trial Participants: 928 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Predicting not just if, but also when, cognitively unimpaired individuals are likely to develop onset of Alzheimer's disease (AD) symptoms would be useful to clinical trials and, eventually, clinical practice. 2 key findings →
Design: cohort Participants: 603 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In the UGOT cohort, the optimal cutoff improved diagnostic accuracy compared with the standard single cutoff, particularly in CKD and anemia (CKD: from 0.65; 95% CI, 0.57-0.72; to 0.83; 95% CI, 0.76-0.89; anemia: from 0.80; 95% CI, 0.76-0.84; to 0.86; 95% CI, 0.82-0.90), with consistent findings in the Roche cohort. 4 key findings →
Design: cross-sectional Participants: 2,571 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Prion diseases can mimic Alzheimer disease (AD) at presentation. 4 key findings →
Design: cohort study Participants: 345 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 1,345 individuals were included. 5 key findings →
Design: cohort study Participants: 1,345 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Copy-number variants (CNVs) are major contributors to human disease. 2 key findings →
Design: case-control Participants: 22,319 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia diagnosis increasingly relies on blood-based biomarkers, yet their performance in diverse populations remains insufficiently characterized. 1 key finding →
Design: cross-sectional Participants: 605 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
< 0.01). Using an operationalization of clinical criteria for LATE, 8.2% of participants with MCI or dementia from our tertiary memory clinic were classified as Possible-LATE, Probable-LATE, or LATE-AD. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Collectively, plasma biomarker findings in the low p-tau217 subgroup were more robust than in the mITT population. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This study estimated the utilization and lifetime costs of formal care for AD dementia using longitudinal register data. 4 key findings →
Design: cohort Participants: 20,366 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
With blood-based phosphorylated tau biomarkers soon to be used for diagnosis of Alzheimer disease, analyzing tau levels in other conditions could enhance biomarker interpretability. 4 key findings →
Participants: 27 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The study included 560 amyloid-positive participants (BioFINDER: n = 431; mean [SD] age, 73.6 [7.0] years; 212 female [49.2%] and 219 male [51.8%]; TRIAD: n = 129; mean [SD] age, 70.4 [8.3] years; 76 female [58.9%] and 53 male [41.1%]). 5 key findings →
Design: cohort study Participants: 431 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This cross-sectional study evaluates the performance of the US Food and Drug Administration–cleared phosphorylated tau 217 (p-tau217) to β-amyloid 42 ratio cut points used to detect amyloid pathology associated with Alzheimer disease. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Sleep spindles (SPs) and slow oscillations (SOs) are linked to cognition and neurodegeneration; however, their relationship with CSF orexin concentrations in symptomatic AD has not been characterized. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed. 4 key findings →
Design: case-control study Participants: 231 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The final study sample comprised 8,797 participants (53.5% women, mean age at HUNT4 77.8 [SD 6.2]). 5 key findings →
Participants: 8,797 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Among 203 enrolled patients, 186 (mean [SD] age, 68.7 [5.2] years; 119 males [64.0%]) were randomized (137 to the CN-105 group, 49 to the placebo group) and underwent surgery. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The study describes 4 males who developed dementia following confirmed or suspected c-hGH treatment in childhood (age at symptom onset between 47 and 60 years) with cognitive syndromes characterized by prominent language involvement. 4 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Individuals with autosomal dominant Alzheimer's disease (ADAD) arising from mutations in PSEN1, PSEN2, or APP exhibit variability in clinical presentation. 4 key findings →
Participants: 2,338 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) develops over a prolonged asymptomatic phase marked by silent pathology. 1 key finding →
Participants: 102 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
They are often found in middle-aged individuals and are associated with a greater risk of stroke and vascular dementia. 5 key findings →
Participants: 1,072 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood-based biomarkers (BBMs) for Alzheimer disease (AD) offer widely expanded access to biomarker-informed diagnoses in community settings that have previously lacked such resources. 1 key finding →
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,040 records (3.4% of the library) are not peer-reviewed — 965 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events