28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Elevated plasma neurofilament light chain (NfL) is associated with dementia though underlying mechanisms remain unknown. 3 key findings →
Design: cross-sectional Participants: 179 Evidence: moderate
Full summary, score breakdown and related studies → Original source
BackgroundDiabetes has been linked to increased prevalence of dementia, but the link between diabetic retinopathy (DR) and Alzheimer's disease (AD) remains unclear. 4 key findings →
Design: cross-sectional Participants: 79 Evidence: low
Full summary, score breakdown and related studies → Original source
The study included 44 iRBD patients (81.8% males, mean age 71.0 ± 6.4 years), 55 HC (66.3% males, mean age 69.1 ± 5.5 years), and 28 AD patients (82.1% males, mean age of 70.4 ± 6.7 years). iRBD patients showed significantly higher plasma NfL and GFAP levels and similar pTau181 levels compared to HC. 5 key findings →
Design: cross-sectional Participants: 44 Evidence: low
Full summary, score breakdown and related studies → Original source
White matter hyperintensities (WMH) is mainly caused by cerebrovascular injury and may also increase the possibilities of progression to Alzheimer's disease. 2 key findings →
Design: cross-sectional Participants: 1,029 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In vitro studies of autosomal dominant Alzheimer's disease implicate longer amyloid-β peptides in disease pathogenesis; however, less is known about the behaviour of these mutations in vivo. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Biomarkers were correlated with one another. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Regular physical activity was positively associated with CSF Aβ42 (p < 0.001) and Aβ42/40 (p < 0.001), while it was negatively associated with p-tau/Aβ42 (p < 0.001) and t-tau/Aβ42 (p < 0.001). 5 key findings →
Design: cross-sectional Participants: 918 Evidence: low
Full summary, score breakdown and related studies → Original source
Only the Aβ negative MCI group (MCI-Aβ-) was associated with depressive symptoms (odds ratio [OR] = 2.65, p = 0.005). 4 key findings →
Participants: 160 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Lumipulse and IP-MS Aβ42/40 exhibited the highest diagnostic accuracy for detecting an abnormal amyloid-PET (areas under the curve [AUCs] of 0.81 and 0.84, respectively). 5 key findings →
Participants: 179 Evidence: low
Full summary, score breakdown and related studies → Original source
The CSF A/T profiles included 49 A+/T+, 8 A+/T-, and 41 A-/T-. 5 key findings →
Design: cross-sectional Participants: 98 Evidence: low
Full summary, score breakdown and related studies → Original source
At a care setting-agnostic cutoff of 0.934 pg/ml, high negative predictive value (NPV) (93.8%) and acceptable positive predictive value (PPV) (46.6%) were observed against amyloid-positron emission tomography (PET). 4 key findings →
Participants: 604 Evidence: low
Full summary, score breakdown and related studies → Original source
Of the 859 participants enrolled in this ongoing study, 20.6% self-identified as Black or African American. 5 key findings →
Participants: 859 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 337 participants were included: 136 ND, 77 PPD, and 124 Controls. 5 key findings →
Participants: 337 Evidence: low
Full summary, score breakdown and related studies → Original source
This study directly compared four different commercial/lab p-tau217 blood tests (Lumipulse, ALZpath, Johnson & Johnson, and NULISA) in 344 people from two community cohorts, most of whom were cognitively normal or had only mild changes. 4 key findings →
Design: cross-sectional Participants: 344 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This cross-sectional evaluation of the NIA-AA criteria for preclinical AD indicates that the 1-3 staging criteria coupled with stage 0 and SNAP categories classify 97% of CN subjects from a population-based sample, leaving only 3% unclassified. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios are significantly better than CSF Aβ42 to detect brain amyloid deposition in prodromal AD and to differentiate AD dementia from non-AD dementias. 5 key findings →
Participants: 1,182 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This roughly 15-year interval where the slope of the amyloid SUVR vs time curve is greatest and roughly linear represents a large therapeutic window for secondary preventive interventions. 1 key finding →
Participants: 246 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Clinical phenotypes are associated with differential patterns of tau but not amyloid pathology. 3 key findings →
Participants: 119 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We observed no differences in plasma AD biomarker levels between AA and NHW participants. 5 key findings →
Participants: 267 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Elecsys-derived CSF biomarkers detect AD neuropathologic changes with very high discriminative accuracy in vivo. 2 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Global PET amyloid burden was compared with regards to cognitive status, APOE ɛ4 status, sex, age, and estimated years to symptom onset. 2 key findings →
Design: cross-sectional Participants: 216 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results suggest that plasma biomarkers can augment detection of preclinical AD among asymptomatic individuals and improve the specificity of AD diagnosis. 1 key finding →
Design: cross-sectional Participants: 746 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In patients with early PD, CSF p-tau 181 and t-tau were low compared with those in controls and did not increase over 5 years of follow-up. 3 key findings →
Design: longitudinal study Participants: 32 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
It has been suggested that the diagnostic landscape of Alzheimer disease (AD) is undergoing a profound transformation, marked by a shift toward a biomarker-based approach, as proposed by the Revised Criteria for Diagnosis and Staging of Alzheimer's Disease. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In the longitudinal analysis of p-tau181 trajectories of the AD+P group, the group of patients who showed incidence of psychosis over the course of follow-up (AD+P incident) demonstrated an associated increase in plasma p-tau181 levels compared with the group of patients who had psychosis at baseline (AD+P baseline) and showed an associated decrease in plasma p-tau181 levels (F4, 117 = 3.24; P = .01). 4 key findings →
Design: cohort study Participants: 752 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 →