OptPRS predicted AD dementia and Aβ positivity, independent of apolipoprotein E (APOE). 5 key findings →
Participants: 1,634 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.
52/100
Two ABCA7 missense variants (rs3764647 and rs3752239) demonstrated significant association with AD risk. 4 key findings →
Participants: 319 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Thirteen pathway clusters were identified, and eight pathway-specific PRSs were significantly associated with AD diagnosis. 5 key findings →
Participants: 1,411 Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenic relevance in Alzheimer's disease (AD) presents a decrease of cerebrospinal fluid amyloid-ß42 (Aß42) burden and an increase in cerebrospinal fluid total tau (T-tau) levels. 3 key findings →
Participants: 843 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Using the data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), we performed a genome-wide association study (GWAS) between 565,373 single nucleotide polymorphisms (SNPs) and 16 key AD biomarkers from 1,576 subjects at four visits. 5 key findings →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, several studies have investigated the association between the rare mutation of triggering receptor expressed on myeloid cells 2 (TREM2) gene (rs75932628-T) and the risk of late-onset Alzheimer's disease (LOAD), but they did not draw the same conclusion. 5 key findings →
Participants: 786 Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
We identified 7 functional variants in APP/PSENs in 8 patients, including 1 APP mutation (p. Val715Met), 3 PSEN1 mutations (p. Phe177Ser; p. Arg377Met; p. Ile416Thr), and 3 PSEN2 mutations (p. Glu24Lys; p. Gly34Ser; p. Met239Thr). 5 key findings →
Participants: 34 Evidence: low
Full summary, score breakdown and related studies → Original source
Transcriptomics and polygenic risk analysis position resilience as an intermediate AD state. 5 key findings →
Participants: 631 Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulation of sphingomyelin and ceramide metabolism have been implicated in Alzheimer's disease. 1 key finding →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
Subjects without amyloid, including three with pathologically confirmed corticobasal degeneration, showed greater regional 18F-AV-1451 retention and associated regional atrophy in areas commonly associated with corticobasal degeneration pathology than healthy control subjects [retention was higher compared to healthy controls (P = 0.0011), driven especially by the precentral gyrus (P = 0.011) and pallidum (P < 0.0001), and greater atrophy was seen in subjects compared to control subjects (P = 0.0004)]. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
[18F]Flortaucipir BPND images showed overall highest binding in the symptomatic carriers. 5 key findings →
Participants: 52 Evidence: low
Full summary, score breakdown and related studies → Original source
The z-scores of perfusion-weighted images of both tracers showed high correlations across the brain, especially in the frontal and parietal lobes, which were the brain regions with pronounced perfusion deficit in the patient group (R = 0.83 ± 0.08; range, 0.61-0.95). 4 key findings →
Participants: 64 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Global visual scores were reliable, correlated with global cortical 18F-flortaucipir standardized uptake value ratio (SUVR) and were associated with clinical diagnosis and amyloid status. 3 key findings →
Participants: 274 Evidence: low
Full summary, score breakdown and related studies → Original source
Percentage of visually tau-positive scans increased with amyloid-beta deposition measured in 18F-florbetaben Centiloids (CL) (7.7% (<36 CL), 80% (>83 CL)). 18F-PI-2620 standardized uptake value ratio (SUVR) was correlated with increased 18F-florbetaben CL in several regions of interest. 5 key findings →
Design: clinical trial Participants: 74 Evidence: low
Full summary, score breakdown and related studies → Original source
Accurate staging of Alzheimer's disease (AD) pathology is crucial for therapeutic trials and prognosis, but existing fluid biomarkers lack specificity, especially for assessing tau deposition severity, in amyloid-beta (Aβ)-positive patients. 2 key findings →
Participants: 136 Evidence: low
Full summary, score breakdown and related studies → Original source
Polynomial regressions indicated an 0.23 kg/m2 decrease in BMI per year beginning at age 36.5 years, which occurs alongside the period during which Aβ and tau increase and memory and mental status decline. 3 key findings →
Participants: 77 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In the smallest required sample of 15 cAD and 10 Aβ-negative participants, conversion error was 1.7 Centiloids at 25 Centiloids and 3.4 Centiloids at 100 Centiloids. 5 key findings →
Participants: 157 Evidence: low
Full summary, score breakdown and related studies → Original source
There is greater interest in amyloid biomarker for the diagnosis of Alzheimer disease (AD) with the recent Food and Drug Administration approval of amyloid-targeted therapy. 1 key finding →
Participants: 74 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
Both MRI-based and CT-based rdcCL scales showed that FMM and FBB were highly correlated with each other, globally and regionally (R2 = 0.96~0.99). 5 key findings →
Participants: 63 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Based on retrospective data, we develop personalized risk estimates for MCI patients. 4 key findings →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid positron emission tomography ([18F] florbetaben (FBB) PET) can be used to determine concomitant Alzheimer's disease (AD) in idiopathic normal pressure hydrocephalus (iNPH) patients. 4 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source
All Centiloid cut-offs fell within the range of 25-35, except for CSF Aβ42 that rendered an optimal cut-off value of 12 CL. 5 key findings →
Participants: 205 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Despite high correlations (GCA: R2 ≥ 0.85), large overestimation and proportional bias of SUVR relative to DVR was observed. 5 key findings →
Participants: 90 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Compared with manual step-by-step processing, our developed automated quantification tool reduced processing time by 85%. 5 key findings →
Participants: 166 Evidence: low
Full summary, score breakdown and related studies → Original source
Reimbursement of amyloid-positron emission tomography (PET) is lagging due to the lack of definitive evidence on its clinical utility and cost-effectiveness. 5 key findings →
Evidence: high
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 →