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Garger, D.

Publications and source records attributed to Garger, D..

2 recordsLinked to original sources

The Interpretable Multimodal Machine Learning (IMML) framework reveals pathological signatures of distal sensorimotor polyneuropathy

Distal sensorimotor polyneuropathy (DSPN) is a common neurological disorder in elderly adults and people with obesity, prediabetes and diabetes and is associated with high morbidity and premature mortality. DSPN is a multifactorial disease and not fully understood yet. Here, we developed the Interpretable Multimodal Machine Learning (IMML) framework for predicting DSPN prevalence and incidence based on sparse multimodal data. Exploiting IMMLs interpretability further empowered biomarker identification. We leveraged the population-based KORA F4/FF4 cohort including 1,091 participants and their deep multimodal characterisation, i.e. clinical data, genomics, methylomics, transcriptomics, proteomics, inflammatory proteins and metabolomics. Clinical data alone is sufficient to stratify individuals with and without DSPN (AUROC = 0.752), whilst predicting DSPN incidence 6.5{+/-}0.2 years later strongly benefits from clinical data complemented with two or more molecular modalities (improved {Delta}AUROC >0.1, achieved AUROC of 0.714). Important and interpretable features of incident DSPN prediction include up-regulation of proinflammatory cytokines, down-regulation of SUMOylation pathway and essential fatty acids, thus yielding novel insights in the disease pathophysiology. These may become biomarkers for incident DSPN, guide prevention strategies and serve as proof of concept for the utility of IMML in studying complex diseases.

bioinformatics↗

Receptor endocytosis orchestrates the spatiotemporal bias of β-arrestin signaling

The varying efficacy of biased and balanced agonists is generally explained by the stabilization of different active receptor conformations. In this study, systematic profiling of transducer activation of AT1 angiotensin receptor agonists revealed that the extent and kinetics of {beta}-arrestin binding exhibit substantial ligand-dependent differences, which however completely disappear upon the inhibition of receptor internalization. Even weak partial agonists for the {beta}- arrestin pathway acted as full or near full agonists, if receptor endocytosis was prevented, indicating that receptor conformation is not an exclusive determinant of {beta}-arrestin recruitment. The ligand-dependent variance in {beta}-arrestin translocation at endosomes was much larger than it was at the plasma membrane, showing that ligand efficacy in the {beta}-arrestin pathway is spatiotemporally determined. Experimental investigations and mathematical modeling demonstrated how multiple factors concurrently shape the effects of agonists on endosomal receptor-{beta}-arrestin binding and thus determine the extent of bias. Among others, ligand dissociation rate and G protein activity have particularly strong impact on receptor-{beta}-arrestin interaction, and their effects are integrated at endosomes. Our results highlight that endocytosis forms a key spatiotemporal platform for biased GPCR signaling and can aid the development of more efficacious functionally-selective compounds. One Sentence summaryAgonist-specific differences in {beta}-arrestin recruitment are mainly determined by the ligand dissociation rate and G protein activation at the endosomes.

cell biology↗