Oxidative Stress and Neurodegenerative Disorders II

Dear Colleagues,

Increased oxidative stress levels have been found to greatly contribute to the onset and progression of neurodegenerative disorders, i.e., Alzheimer’s disease, Parkinson’s disease, Down syndrome, amyotrophic lateral sclerosis (ALS), and Huntington disease. The loss of physiological equilibrium between antioxidant and pro-oxidant stimuli, which normally contribute to the maintenance of low free radical levels, leads to increased generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) that are toxic for brain cells in several ways. Indeed, augmented ROS and RNS production is responsible for damage to proteins, lipids, and nucleic acids, which accumulates within the cells and disrupts cellular homeostasis. Perturbation of mitochondrial activity further boosts ROS and RNS production, finally resulting in impaired metabolic pathways normally fueling brain cells’ energetic needs. In this frame, neurons display a distinctive bioenergetic metabolism, characterized by  a particularly elevated mitochondrial oxygen consumption rate to sustain the high ATP (energy) expenditure. These features contribute to the exquisite sensitivity of the brain to the detrimental effects of oxidative stress. Recent findings suggest the crucial role of metabolic networks in the regulation of neuronal tolerance against oxidative stress. Furthermore, emerging evidence highlights the impact of metabolism and redox signaling on the genetic and epigenetic regulation of gene expression. Collectively, these elements indicate the extraordinary complexity of the multileveled molecular mechanisms deployed by brain cells to cope with oxidative stress.

This Special Issue will discuss preclinical and clinical evidence highlighting the central role of oxidative stress in the progression of neurodegenerative disorders and the strategies currently adopted to protect the brain.

Prof. Dr. Eugenio Barone
Dr. Andres Trostchansky
Guest Editors

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