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Alferink, J.

Publications and source records attributed to Alferink, J..

3 recordsLinked to original sources

Multi-Methodological Characterization of Sleep Deprivation: From Standard EEG Power Spectra to Aperiodic Dynamics in Humans and Mice.

Sleep deprivation is a potent, rapid-acting therapeutic intervention for major depressive disorder, yet its underlying neural mechanisms remain poorly understood, hindering the development of predictive biomarkers. Here, we systematically characterize the electro-physiological signatures of prolonged wakefulness using a multi-methodological approach across three independent datasets in humans and mice. By integrating standard power spectral density analysis with aperiodic component fitting (SpecParam) and highly compar-ative time-series analysis (HCTSA), we identified robust cross-species biomarkers of sleep pressure. Machine learning models revealed that theta power is the most consistent feature for differentiating control and sleep deprivation states, achieving up to 90% classification accuracy. Sleep deprivation significantly increased the spectral offset - suggesting global cortical hyperexcitation - while simultaneously steepening the spectral slope. We interpret this simultaneous shift as a state uncoordinated state of hyperexcited and inefficient neu-ral processing. These findings establish reproducible EEG markers of sleep deprivation that transcend species. Given the clinical utility of wake therapy, we propose that prefrontal the-ta power and spectral offset/slope may serve as mechanism-based predictors of therapeu-tic response. Our results provide a framework for the clinical validation of these biomarkers, potentially enabling personalized chronotherapeutic interventions for psychiatric disorders.

neuroscience↗

BATF controls IFN I production via DC-SCRIPT in plasmacytoid dendritic cells

The basic leucine zipper ATF-like transcription factor (BATF) plays a pivotal role in coordinating various aspects of lymphoid cell biology, yet essential functions in dendritic cells (DCs) have not been reported. Here we demonstrate that BATF deficiency leads to increased interferon (IFN) I production in Toll-like receptor 9 (TLR9)-activated plasmacytoid dendritic cells (pDCs), while BATF overexpression has an inhibitory effect. BATF-deficient mice exhibit elevated IFN I serum levels early in lymphocytic choriomeningitis virus (LCMV) infection. Through ATAC-Seq analysis, BATF emerges as a pioneer transcription factor, regulating approximately one third of the known transcription factors in pDCs. Integrated transcriptomics and ChIP-Seq approaches identified the transcriptional regulator DC-SCRIPT as a direct target of BATF that suppresses IFN I promoter activity by interacting with the interferon regulatory factor 7 (IRF7). Genome-wide association study (GWAS) analyses further implicate BATF in pDC-mediated human diseases. Our findings establish a novel negative feedback axis in IFN I regulation in pDCs during anti-viral immune responses orchestrated by BATF and DC-SCRIPT, with broader implications for pDC and IFN I-mediated autoimmunity.

immunology↗

The transcription factor reservoir and chromatin landscape in activated plasmacytoid dendritic cells

Transcription factors (TFs) control gene expression by direct binding to regulatory regions of target genes but also by impacting chromatin landscapes and thereby modulating DNA accessibility for other TFs. To date, the global TF reservoir in plasmacytoid dendritic cells (pDCs), a cell type with the unique capacity to produce unmatched amounts of type I interferons, has not been fully characterized. To fill this gap, we have performed a comprehensive analysis in naive and TLR9-activated pDCs in a time course study covering early timepoints after stimulation (2h, 6h, 12h) integrating gene expression (RNA-Seq), chromatin landscape (ATAC-Seq) and Gene Ontology studies. We found that 70% of all described TFs are expressed in pDCs for at least one stimulation time point and that activation predominantly "turned on" the chromatin regions associated with TF genes. We hereby define the complete set of TLR9-regulated TFs in pDCs. Further, this study identifies the AP-1 family of TFs as potentially important but so far less well characterized regulators of pDC function.

molecular biology↗