30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Analyses measured the associations between predictor variables and the memory score, and whether AT(N) biomarker profiles significantly improved prediction of memory z score rates of change beyond a model with clinical and genetic variables only. 3 key findings →
Design: cohort study Participants: 480 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CKD was associated with increased p-tau217 concentrations when measuring p-tau217 by ALZpath and C 2 N methodologies, but the effect was mitigated by the use of %p-tau217. 5 key findings →
Design: cross-sectional Participants: 202 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In persons selected from a population-based study, elevated amyloid levels at baseline were associated with worse cognition and imaging biomarkers at baseline and with greater clinical decline and neurodegeneration. 5 key findings →
Design: longitudinal study Participants: 286 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Vascular health had quantifiably greater impact on neurodegeneration in AD regions than on amyloid deposition. 3 key findings →
Design: longitudinal study Participants: 430 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our transition rates suggest that brain ageing is a nearly inevitable acceleration toward worse biomarker and clinical states. 5 key findings →
Design: cross-sectional Participants: 4,049 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There were minimal effects of lifestyle enrichment on AD biomarker trajectories (specifically rates). 5 key findings →
Design: longitudinal study Participants: 393 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
GFAP was associated with amyloid and tau PET in multivariable models. 4 key findings →
Design: cross-sectional Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
MRI and CSF provide complimentary predictive information about time to conversion from amnestic mild cognitive impairment to Alzheimer disease and combination of the 2 provides better prediction than either source alone. 3 key findings →
Participants: 399 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found no significant correlation between CSF biomarkers and cognitive scores in any of the 3 clinical groups individually. 2 key findings →
Design: cross-sectional Participants: 399 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The plasma Abeta42/Abeta40 ratio may be a useful premorbid biomarker for identifying cognitively normal elderly white subjects who are at increased risk for developing MCI or AD. 5 key findings →
Participants: 53 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This study provides a systematic framework for selection of assay-specific cutpoints for clinical use of plasma p-tau217 for determination of amyloid status. 4 key findings →
Participants: 427 Evidence: low
Full summary, score breakdown and related studies → Original source
Low CSF Abeta(1-42) (surrogate for Abeta amyloid load) is more closely linked to the presence of APOE epsilon4 than to clinical status. 3 key findings →
Participants: 399 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Unlike the CSF biomarkers evaluated, changes in serial structural MRI are correlated with concurrent change on general cognitive and functional indices in impaired subjects, track with clinical disease stage, and are influenced by APOE genotype. 3 key findings →
Participants: 312 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
None of the lifestyle variables were correlated with the biomarkers, and the path associations between lifestyle variables and biomarkers were not significant (p > 0.05). 3 key findings →
Participants: 515 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We evaluated the relationship between baseline CSF p-tau181 and the rate of tau PET change in the temporal meta-ROI and entorhinal cortex (ERC) and how it varied by amyloid level (CSF Aβ42 or amyloid PET) among 143 individuals from the Mayo Clinic Study of Aging and Mayo Alzheimer Disease Research Center. 3 key findings →
Design: longitudinal study Participants: 143 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Amyloidosis in the absence of neurodegeneration did not have an adverse impact on practice effects or the 30-month cognitive trajectories. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We recently demonstrated that the frequencies of biomarker groups defined by the presence or absence of both amyloidosis (A+) and neurodegeneration (N+) changed dramatically by age in cognitively non-impaired subjects. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
A reduction in plasma Aβ 42 /Aβ 40 is associated with an increased risk of subsequent epilepsy. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cognitively normal persons with brain injury biomarker abnormalities, with or without abnormal levels of β-amyloid, were indistinguishable on a variety of imaging markers, clinical features, and risk factors. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers such as phospho-tau species are increasingly used in clinical practice for the diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Multiple variables affect plasma biomarkers of amyloid pathology and neurodegeneration among CU in the general population. 3 key findings →
Evidence: low
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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