Publications by authors named "K Gehring"
Parkinson disease (PD) is a neurodegenerative disease characterized by the loss of dopaminergic neurons in the , primarily due to mitochondria dysfunction. PRKN (parkin RBR E3 ubiquitin protein ligase) and PINK1 (PTEN induced kinase 1) are linked to early-onset cases of PD and essential for the clearance of damaged mitochondria via selective mitochondrial autophagy (mitophagy). In a recent publication, we detail how a small molecule can activate PRKN mutants that are unable to be phosphorylated, restoring mitophagy in cellular assays.
View Article and Find Full Text PDFMutations in the E3 ubiquitin ligase parkin cause a familial form of Parkinson's disease. Parkin and the mitochondrial kinase PTEN-induced kinase 1 assure quality control of mitochondria through selective autophagy of mitochondria (mitophagy). Whereas numerous parkin mutations have been functionally and structurally characterized, several Parkinson's disease mutations found in the catalytic Rcat domain of parkin remain poorly understood.
View Article and Find Full Text PDFArticle Synopsis
- Computerized neuropsychological test batteries (CNTs), like Central Nervous System Vital Signs (CNS VS), are common for assessing cognitive function, but there's little proof that they effectively measure cognition.
- In studying the factor structure of CNS VS across various samples (healthy adults and patients with different types of brain tumors), researchers found differences in how factors were interpreted based on health status.
- Overall, the findings suggest that the current "clinical domains" of CNS VS may not be valid, and it's better for researchers and clinicians to rely on individual test scores rather than total sum scores.
Article Synopsis
- Mutations in parkin and PINK1 lead to early-onset Parkinson's disease by impairing the process of removing damaged mitochondria, where parkin is activated by PINK1 to ubiquitinate and target these organelles for degradation.* -
- Researchers discovered a new class of small molecules that enhance parkin's activity by acting as molecular glues, which improve the interaction between phospho-ubiquitin and parkin.* -
- The most effective compound, BIO-2007817, has been shown to partially restore parkin activity in specific EOPD mutants, suggesting potential therapeutic applications for treating Parkinson's disease.*