Thomas Nickl‐Jockschat

This study investigates whether pupil dilation, a measure of autonomic response to errors, causally influences conscious error detection in older adults using atomoxetine.

This study shows that Ube3a gene overdosage causes sex-biased effects on brain connectivity, behavior, and gene expression in mice, linking it to autism-related phenotypes.

This study uses machine learning to define the transcriptomic architecture of the human cerebral cortex, revealing a multi-resolution organization and identifying core regions linked to higher cognitive functions.

This study identifies sex- and cell type-specific transcriptomic and behavioral effects of 16p11.2 hemideletion in mice, revealing distinct impacts on striatal circuits and locomotor behavior.

This study identifies three genes in the 16p11.2 region that replicate sex-specific striatal phenotypes of 16p11.2 hemi-deletion in mice through CRISPR/Cas9-generated 3g del/+ mice.

This study uses spatial transcriptomics to show that sleep deprivation causes region-specific gene expression changes in the brain, with the hippocampus showing the most significant alterations.

This study shows that naltrexone prevents neuroinflammation and epileptogenesis in a mouse model of post-traumatic epilepsy.

This study identifies the gene expression changes in the human brain following electrical stimulation, revealing non-neuronal cell involvement and a conserved gene signature.

This study shows that type I interferon signaling worsens neuropathology and neurologic dysfunction after traumatic brain injury by modulating neuroimmune responses.

This study identifies the lateral septum as a key circuit involved in ketamine-induced social deficits, showing that its hypoactivation contributes to schizophrenia-like behaviors.

The paper identifies five major transcriptional patterns of brain disease risk genes across the adult human brain and highlights species-specific differences in psychiatric and substance abuse-related diseases.

The paper predicts individual schizophrenia symptom dimensions using functional brain networks and links these networks to molecular features like dopamine and serotonin systems.

The paper identifies clinically relevant genetic dysfunction in ASD risk genes by analyzing whole-exome data from 2,381 individuals, finding associations between specific variants and cognitive symptoms.