Different information sources yield widely varied prevalence and expenditure estimates. 1 key finding →
Participants: 57,669 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The use of methods that focus on determining a single underlying cause may lead to underestimation of the extent of the contribution of some diseases such as dementia and respiratory disease to death in older adults and overestimation of the contribution of other diseases. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Comorbidities in community-living older adults with dementia are common and account for a substantial proportion of health service use and costs in this population. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Claims data studies that include indicators of potentially diminished patient functional status better capture heterogeneity of patients with multiple chronic conditions. 1 key finding →
Participants: 72,056 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Due to complex relationships of body-mass index and blood pressure with dementia individual components cancelled each other out and rendered the sum-scores meaningless for the prediction of dementia. 5 key findings →
Participants: 3,547 Evidence: low
Full summary, score breakdown and related studies → Original source
Changing instructions while maintaining the same cognitive and motor tasks on WWT in older adults result in task prioritization effects. 5 key findings →
Design: cross-sectional Participants: 189 Evidence: low
Full summary, score breakdown and related studies → Original source
We developed prediction rules to guide the clinical diagnosis of Alzheimer's disease (AD) in two community-based cohort studies (the Religious Orders Study and the Rush Memory and Aging Project). 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated tau species have been recently proposed as peripheral markers of Alzheimer's disease (AD) pathology. 4 key findings →
Design: cross-sectional Participants: 91 Evidence: low
Full summary, score breakdown and related studies → Original source
Four subtypes were identified: limbic, medial temporal lobe (MTL) sparing, posterior, and lateral temporal (l temporal). 5 key findings →
Participants: 606 Evidence: low
Full summary, score breakdown and related studies → Original source
The clinical utility of plasma phosphorylated tau at threonine 217 (p-tau217) levels as a diagnostic tool for cognitive disorders in real-world settings remains uncertain. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
aECAD was associated with significantly worse scores in processing speed (β = -0.19, p = 0.004) and executive function (β = -0.20, p = 0.009) domains after controlling for age, sex, education, race, and ethnicity. 3 key findings →
Participants: 182 Evidence: low
Full summary, score breakdown and related studies → Original source
Estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2, cardiovascular disease (CVD), and amyloid- and tau-PET-positive status demonstrated higher p-tau217. 5 key findings →
Participants: 233 Evidence: low
Full summary, score breakdown and related studies → Original source
Both Mann-Whitney tests and ANCOVA found significant differences between groups racialized as AA or NWH with respect to global 11[C]-Pittsburgh Compound B (PiB) standardized uptake value ratio (SUVR), cortical thickness values, p-tau181, and p-tau231 values (p < 0.05). 3 key findings →
Participants: 260 Evidence: low
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
In total, samples from 610 individuals from four clinical centres were investigated in this study. 5 key findings →
Participants: 230 Evidence: low
Full summary, score breakdown and related studies → Original source
VRFs and gait were associated with diffusion changes even in low age strata. 5 key findings →
Participants: 745 Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofilaments are structural components of neurons and are particularly abundant in highly myelinated axons. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Significant interaction effects were observed: MoCA (β = -1.86×10-4, P = 0.006) and PACC (β = -4.0×10-5, P = 0.004), indicating HDL moderates the negative association between NfL and cognition. 3 key findings →
Participants: 417 Evidence: low
Full summary, score breakdown and related studies → Original source
Major depressive disorder (MDD) has been associated with an increased risk of cognitive decline and neurodegenerative disorders like Alzheimer's disease (AD), prompting interest in peripheral biomarkers related to amyloid metabolism as well as neuroaxonal and astroglial injury. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genetic investigations and associations with plasma biomarkers of dementia with Lewy bodies (DLB) in East Asian populations are lacking. 4 key findings →
Participants: 151 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Over 3.7 years, 22 patients phenoconverted (7 multiple system atrophy [MSA]; 15 Lewy body diseases [LBDs]). 5 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
Baseline NfL and GFAP did not differ between patients with or without ARIA (ln[NfL] ECLIA 1.24 ± 0.38 pg/mL vs 1.25 ± 0.40 pg/mL, p = 0.77; ln[NfL] Simoa 2.87 ± 0.47 pg/mL vs 2.98 ± 0.40 pg/mL, p = 0.30, ln[GFAP] ECLIA 4.95 ± 0.36 pg/mL vs 4.88 ± 0.47 pg/mL, p = 0.69). 4 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies demonstrated that plasma neurofilament light chain (NFL) played important predictive roles in disease progression and neurodegeneration in the preclinical phase of familial Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Comparing those having MCI, both CU and SCD participants had significantly lower amyloid PET standardized uptake value ratio (SUVR) (p < 0.001; p = 0.005). 4 key findings →
Participants: 66 Evidence: low
Full summary, score breakdown and related studies → Original source
55/100
Besides age and estimated glomerular filtration rate (eGFR), significant associations were found between plasma biomarkers and clusters related to hemoglobin, red blood cell distribution, and inflammation. 5 key findings →
Participants: 305 Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →