Topic: mitochondrial ROS

Parkinson's disease (PD) is a multifaceted neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons, predominantly within the substantia nigra pars compacta (SNc) region. Dysregulation of FoxO1 has been implicated in various neurodegenerative diseases, including Alzheimer's disease and PD, yet the precise underlying mechanisms remain largely elusive. In this study, we investigated the impact of α-synuclein pre-formed fibrils (PFF) treatment on BV-2 microglial cells to elucidate alterations in molecular properties and neuronal degeneration. Surprisingly, our find

Perturbations in brain cell metabolism are consistently interwoven with neurodegenerative disorders like Alzheimer's disease (AD)(1). In particular, dysfunctions of mitochondrial bioenergetics incite severity of AD pathology (2), whereas proof-of-concept evidence indicates that glutamate can feed mitochondrial ATP synthesis, thereby preventing deadly derangements in Ca2+ and redox homeostasis in different neurodegenerative models (3;4).In this work, we tested a pharmacological approach to stimulate the glutamate dehydrogenase (GDH) function with the allosteric activator 2-Aminobicyclo-(2,2,1)-

Recent advances in understanding the biomolecular mechanisms of sleep control in the Drosophila model have implicated mitochondrial ROS as a key cog in the machine. Hyperkinetic, the beta subunit to the potassium channel Shaker, has been shown to act as a conduit translating rising levels of that mitochondrial ROS during waking hours to heightened cell excitability in the sleep-controlling dorsal fan-shaped body-projecting neurons (dFB) in flies. In order to explore the universality of this mechanism, we instigated a parallel study in mice. Hyperkinetic has three homologs in the mammalian geno