27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We investigated associations of neighborhood disadvantage with Alzheimer's Disease (AD)-related outcomes by biological and social factors in at-risk older adults. 1,880 U.S. POINTER participants with Area Deprivation Index (ADI) and cognition (PACC) were included. 868 had amyloid, tau PET, white matter hyperintensities (WMH), and/or gray matter volumes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The exposome factors, such as diet, lifestyle, microbiome, chemical exposures and social exposome, shapes human health beyond genetic influences, but the mechanisms remain only partially understood. 1 key finding →
Participants: 449 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Symptomatic DIAD participants who had been treated for ∼ 4 years with anti-Aβ monoclonal antibodies (gantenerumab, n=4 or solanezumab, n=4) were compared with untreated, symptomatic DIAD mutation carriers (n=40) and with age-relevant non-DIAD controls with modest or no plaque pathology (n=18). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
GWAS found associations between plasma biomarkers and the APOE gene. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
An extra copy of the amyloid precursor protein gene (APP) is present in Down syndrome (DS) and APP duplication (APPdup), increasing the risk of Alzheimer disease (AD) and cerebral amyloid angiopathy (CAA). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers have expanded access to biologically supported diagnosis of Alzheimer's disease (AD), particularly through measurement of amyloid-beta (Aβ) and phosphorylated tau species1-3. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support a model in which p-tau217 specifically tracks amyloid-driven pathological progression, while markers of neurodegeneration reflect broader age-related processes that are not associated with APOE genotype. 3 key findings →
Design: longitudinal study Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) pathology accumulates years before overt cognitive impairment, yet its multidomain phenotype remains poorly defined. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma pTau217 best identified amyloid-PET positivity (AUC > 0.91). 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Most evidence on dementia risk factors comes from older or clinical samples, leaving their relation to normal cognitive aging unclear. 4 key findings →
Participants: 1,396 Evidence: moderate
Full summary, score breakdown and related studies → Original source
TSE showed stronger unadjusted associations than SUVR in selected region- and outcome-specific comparisons, supporting its potential as a complementary measure. 2 key findings →
Participants: 682 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers for Alzheimer disease and related dementias have been validated largely in populations of European ancestry. 4 key findings →
Participants: 786 Evidence: low
Full summary, score breakdown and related studies → Original source
Key Points Question Which candidate plasma proteins are associated with cognitive performance across multiple domains in older adults from the Democratic Republic of Congo? 5 key findings →
Design: prospective cohort Participants: 779 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma eMTBR-tau243 has been associated with tau pathology and cognitive decline. 3 key findings →
Design: cohort study Participants: 436 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The blood-based biomarker (BBM) profiles associated with genetic susceptibility to Alzheimer’s disease (AD) in general older populations remain poorly understood. 3 key findings →
Participants: 3,947 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid biomarkers sample distinct levels of an open, kinetically coupled biochemical system, yet scalar summaries may obscure biologically relevant configuration. 4 key findings →
Participants: 91 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 is elevated in αSynSAA-positive individuals at equivalent AD pathology measured by amyloid PET or the CSF ratio, and this elevation is attenuated most by fibrillar tau. 2 key findings →
Design: cross-sectional Participants: 193 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support plasma biomarkers for disease identification and risk stratification while underscoring the need for population□specific approaches. 4 key findings →
Participants: 3,645 Evidence: moderate
Full summary, score breakdown and related studies → Original source
ADNI identified task-dependent performance boundaries, particularly attenuated conditional T discrimination within A+. 2 key findings →
Design: post-hoc analysis Participants: 1,097 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Basal ganglia iron serves as a stage-dependent mediator linking pTau217 to hippocampal neurodegeneration, with prodromal AD potentially indicating a particularly vulnerable stage for iron-targeted interventions and iron profiling for patient stratification. 1 key finding →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source
NOS1AP is an adaptor for neuronal nitric oxide synthase that engages several partner proteins and is implicated in Alzheimer’s disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Strong αSyn SAA positivity was detected in 24/443 patients with ALS (5.4%); overall positivity, including weak-positive samples, was 37/443 (8.4%). 5 key findings →
Design: longitudinal study Participants: 248 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We revealed graded, allele dosage‑dependent risk elevations for ACD, AD and VaD among APOE4 carriers, whereby homozygous carriers exhibited substantially higher incident dementia risk relative to heterozygous carriers and non‑carriers across all three clinical endpoints. 5 key findings →
Participants: 58,876 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based neurofilament light (NfL) is associated with all-cause mortality, but whether this reflects neuroaxonal injury or overlaps with cognitive and functional decline remains unclear. 3 key findings →
Participants: 559 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In Phase 1 (n =176), inpatients with delirium showed higher concentrations of both NfL and GFAP than patients with dementia (β = 0.78; 95% CI [0.37, 1.20] and β = 0.39 [0.07, 0.73] respectively) or PPD groups (β = 1.17; [0.69, 1.66] and β = 0.83 [0.51, 1.24] respectively). 5 key findings →
Design: cross-sectional Participants: 176 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →