The Role of the Left Inferior Parietal Cortex in Gilles de la Tourette Syndrome—An rTMS Study

Paulus, Theresa; Wernecke, Lynn; Lundie, Annik; Friedrich, Julia; Verrel, Julius; Rawish, Tina; Weissbach, Anne; Frings, Christian; Beste, Christian; Bäumer, Tobias; Münchau, Alexander

doi:10.3390/biomedicines11030980

Cited by 4 publications

(1 citation statement)

References 38 publications

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“…Increased activity in the left inferior parietal cortex (BA40) appears to be involved in the generation of tics. However, inhibitory repetitive transcranial magnetic stimulation (rTMS) compared to sham and applied to the left prefrontal cortex (BA 40) in 29 adults with TS showed no evidence of benefit on tics (Paulus et al 2023).…”

Section: Other Treatmentsmentioning

confidence: 99%

Tourette syndrome research highlights from 2023

Hartmann,

Andrén,

Atkinson-Clement

et al. 2024

F1000Res

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Section: Other Treatmentsmentioning

confidence: 99%

Tourette syndrome research highlights from 2023

Hartmann,

Andrén,

Atkinson-Clement

et al. 2024

F1000Res

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Comprehensive analysis of epigenetic and epitranscriptomic genes’ expression in human NAFLD

Herranz,

López-Pascual,

Clavería-Cabello

et al. 2023

J Physiol Biochem

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Non-alcoholic fatty liver disease (NAFLD) is a multifactorial condition with a complex etiology. Its incidence is increasing globally in parallel with the obesity epidemic, and it is now considered the most common liver disease in Western countries. The precise mechanisms underlying the development and progression of NAFLD are complex and still poorly understood. The dysregulation of epigenetic and epitranscriptomic mechanisms is increasingly recognized to play pathogenic roles in multiple conditions, including chronic liver diseases. Here, we have performed a comprehensive analysis of the expression of epigenetic and epitranscriptomic genes in a total of 903 liver tissue samples corresponding to patients with normal liver, obese patients, and patients with non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH), advancing stages in NAFLD progression. We integrated ten transcriptomic datasets in an unbiased manner, enabling their robust analysis and comparison. We describe the complete landscape of epigenetic and epitranscriptomic genes’ expression along the course of the disease. We identify signatures of genes significantly dysregulated in association with disease progression, particularly with liver fibrosis development. Most of these epigenetic and epitranscriptomic effectors have not been previously described in human NAFLD, and their altered expression may have pathogenic implications. We also performed a comprehensive analysis of the expression of enzymes involved in the metabolism of the substrates and cofactors of epigenetic and epitranscriptomic effectors. This study provides novel information on NAFLD pathogenesis and may also guide the identification of drug targets to treat this condition and its progression towards hepatocellular carcinoma.

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