28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
18 F-MK-6240 recapitulated Braak staging and correlated with CSF tau and p-tau, normalized to Aβ42 . 18 F-MK-6240 negatively correlated with age across Braak regions in amyloid-positive participants, consistent with greater tau pathology in earlier onset AD. 2 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
In both cohorts, we observed that tau-PET standardized uptake value ratio in medial temporal lobes was associated with clinical dementia rating Sum of Boxes (CDR-SoB) scores independently of local amyloid-PET uptake (FWE corrected at p < 0.001). 5 key findings →
Participants: 154 Evidence: moderate
Full summary, score breakdown and related studies → Original source
GMM-based cutoffs classified less subjects as T+, mainly in the A- CN (<3.4% vs >28.5%) and A+ CN (<14.5% vs >42.9%) groups and showed higher agreement with visual rating (ICC=0.91 vs ICC<0.62) than published cutoffs. 3 key findings →
Participants: 269 Evidence: low
Full summary, score breakdown and related studies → Original source
A subset of participants received cognitive testing and/or the Movement Disorders Society Unified Parkinson's Disease Rating Scale Part III motor exam (off medication). 18F-PI-2620 uptake was low overall in Lewy body disease and correlated with β-amyloid PET in temporal lobe regions and precuneus. 5 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Differential FTP-PET signal patterns showed significant negative associations with domain-specific annual rates of decline. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tau accumulation starts during the preclinical phase of Alzheimer's disease and is closely associated with cognitive decline. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Elevated CSF p-tau181 and cortical 18F-PI-2620 binding was characteristic for AD while normal CSF p-tau181 with elevated subcortical 18F-PI-2620 binding was characteristic for 4RTs. 18F-PI-2620-assessed posterior cortical hypoperfusion could be used as an additional neuronal injury biomarker in AD. 5 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
Data were available from 131 participants with age ranging from 65.4 to 88.2 years and mean follow up of 2.4 years (SD = 1.0). 5 key findings →
Participants: 131 Evidence: low
Full summary, score breakdown and related studies → Original source
Twenty-six percent of participants were PET positive. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain amyloid deposition is one of the main hallmarks of Alzheimer's disease (AD) and two approaches are available for assessing amyloid pathology in vivo: cerebrospinal fluid (CSF) biomarkers levels and amyloid load visualized by amyloid beta positron emission tomography imaging (Amy-PET) probes. 1 key finding →
Participants: 31 Evidence: moderate
Full summary, score breakdown and related studies → Original source
APOEε4 is the most well-established genetic risk factor for sporadic Alzheimer's disease and is associated with cerebral amyloid-β. 4 key findings →
Participants: 211 Evidence: low
Full summary, score breakdown and related studies → Original source
There is both clinical and neuroanatomical variability at the single-subject level in Alzheimer's disease, complicating our understanding of brain-behaviour relationships and making it challenging to develop neuroimaging biomarkers to track disease severity, progression, and response to treatment. 5 key findings →
Participants: 1,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Intergrader agreements for overall 3 × 3 mm image quality and quantitative assessment of VD and FAZ ranged between 71% and 87% (52 images). 5 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source
Subjective cognitive decline (SCD) serves as an initial symptom of preclinical Alzheimer's disease (AD). 4 key findings →
Participants: 57 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Previous studies have explored the associations of retinal vessel calibre, measured from retinal photographs or fundus images using semi-automated computer programs, with cognitive impairment and dementia, supporting the concept that retinal blood vessels reflect microvascular changes in the brain. 3 key findings →
Participants: 212 Evidence: low
Full summary, score breakdown and related studies → Original source
This study investigates various pathological tau isoforms in the retina of individuals with early and advanced Alzheimer's disease (AD), exploring their connection with disease status. 5 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
The SVCI group showed lower CD in the temporal quadrant of the RPC network compared to the CN group (mean (SD), 42.34 (6.29) vs 48.45 (7.08); p = 0.001). 5 key findings →
Design: cross-sectional Participants: 69 Evidence: low
Full summary, score breakdown and related studies → Original source
Serum concentrations of semorinemab were consistent across studies and showed a dose-proportional increase across the evaluated dose range. 5 key findings →
Design: clinical trial Participants: 8,430 Evidence: low
Full summary, score breakdown and related studies → Original source
We identified GLP-1 receptor agonist initiation compared to DPP-4 inhibitors initiation was associated with a reduced risk of AD (hazard ratio [HR] ≤ 0.69 and P value < 0.001) and SGLT-2 inhibitor initiation compared to DPP-4 inhibitor initiation was associated with a reduced risk of AD (HR ≤ 0.67 and P value < 0.001). 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Patients who started ChEI therapy after the introduction of the coverage policy had a significantly longer persistence. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Overall, 74 studies containing 92 cases were found of MDs related to ACHEIs. 5 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
No statistically significant improvement in the primary outcome measures (MMSE and ADAS-Cog) was observed with drug therapy at 36 weeks, at which point all groups had lost, on average, 1 point on the MMSE and gained 2-3 points on the ADAS-Cog scale compared with baseline. 5 key findings →
Participants: 938 Evidence: high
Full summary, score breakdown and related studies → Original source
The objective of this study was to evaluate the relation of metformin with change in cognition and brain pathology. 2 key findings →
Participants: 3,029 Evidence: low
Full summary, score breakdown and related studies → Original source
The outcomes of the present study aim to elucidate the significance of the PDE4 inhibition mechanism as a prospective therapeutic target for enhancing cognitive function in individuals with (a)MCI and mild AD dementia. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
There was no statistically significant difference between the two groups in terms of depressive symptoms, cognitive functions, and ADL. 5 key findings →
Participants: 100 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 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 →