ArticleAlzheimer's & dementia (New York, N. Y.)
Correlations of
Article in Alzheimer's & dementia (New York, N. Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionEarly-onset Alzheimer's disease (EOAD) is mostly caused by mutations in
methodsWe performed pairwise correlations between 276 in vitro functional assays of missense variants from
resultsWe found that VEPs were consistently correlated with age at onset (AAO) among EOAD patients and the amyloid-β (Aβ) 42/Aβ40 ratio biomarker. Regarding the ratio, we observed discrepancies in the predictor variables influencing the Aβ42/Aβ40 ratio, with conflicting evidence as to whether the elevated ratio stems from diminished Aβ40 levels or augmented Aβ42 production. We also identified that with increased predicted pathogenicity, there were decreased Aβ38 levels. Conversely, this study found no direct correlations with Aβ37 and Aβ43. Lastly, structural studies show characteristics of both DN and LoF mechanisms, as there are variants positioned in buried hydrophobic domains and charged surfaces. DISCUSSION: Currently, a major clinical challenge in the field is the lack of reliable approaches for predicting the pathogenicity of variants in EOAD. Our study also illuminates the need for experimental studies to identify the predictor variable causing the increased Aβ42/Aβ40 biomarker. Highlights: We performed correlations of 37 VEPs against in vitro data of EOAD variants.VEPs demonstrate potential as diagnostic tools for early onset Alzheimer's disease.Pathogenic missense variants show characteristics of DN and LoF effects.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.