How EXACTLY is your doctor ensuring oxidative damage from your stroke doesn't occur?
Reactive Oxygen Species: Angels and Demons in the Life ofa Neuron
Kasturi Biswas 1,2 , Kellianne Alexander 1,2 and Michael M. Francis 1,2,*
1 Department of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA;
kasturi.biswas@umassmed.edu (K.B.); kellianne.alexander@umassmed.edu (K.A.)
2 Graduate Program in Neuroscience, Morningside Graduate School of Biomedical Sciences, UMass Chan
Medical School, Worcester, MA 01605, USA
* Correspondence: michael.francis@umassmed.edu
Abstract:
Reactive oxygen species (ROS) have emerged as regulators of key processes supporting
neuronal growth, function, and plasticity across lifespan. At normal physiological levels, ROS
perform important roles as secondary messengers in diverse molecular processes such as regulating
neuronal differentiation, polarization, synapse maturation, and neurotransmission. In contrast, high
levels of ROS are toxic and can ultimately lead to cell death. Excitable cells, such as neurons, often
require high levels of metabolic activity to perform their functions. As a consequence, these cells
are more likely to produce high levels of ROS, potentially enhancing their susceptibility to oxidative
damage. In addition, because neurons are generally post-mitotic, they may be subject to accumulating
oxidative damage. Thus, maintaining tight control over ROS concentration in the nervous system
is essential for proper neuronal development and function. We are developing a more complete
understanding of the cellular and molecular mechanisms for control of ROS in these processes.
This review focuses on ROS regulation of the developmental and functional properties of neurons,
highlighting recent in vivo studies. We also discuss the current evidence linking oxidative damage to
pathological conditions associated with neurodevelopmental and neurodegenerative disorders.
Keywords: synapse; oxidative stress; C. elegans; neuro
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