![]() Since the 1950s and Harman’s Free-radical theory of aging, a compelling amount of research has investigated how ROS and reactive nitrogen species (RNS) influence disease progression. Until recently, ROS were essentially considered to be responsible for significant cellular damages, causing premature aging and neurodegenerative disorders. However, the dark side of energy production is the formation of reactive oxygen species (ROS) as a by-product by the mitochondria’s electron transport chain. Mitochondria are known to fulfill this crucial role, producing the majority of the energy supporting cell growth and homeostasis. Most, if not all, cellular processes require considerable energy. The cellular functions rely on a variety of extracellular signals and intracellular signaling that function in concert to maintain cellular homeostasis. This review provides an overview of ROS function in cell signaling in the context of aging and degeneration in the brain and guarding the fragile balance between health and disease. In the brain, their impact on neurons and astrocytes has been associated with synaptic plasticity and neuron survival. ROS are active actors in most of the signaling cascades involved in cell development, proliferation and survival, constituting important second messengers. More recent research suggests more complex function of ROS, reaching far beyond the cellular dysfunction. ROS were first identified as by-products of the cellular activity, mainly mitochondrial respiration, and their high reactivity is linked to a disruption of macromolecules such as proteins, lipids and DNA. Reactive oxygen species (ROS) have been closely associated with health decline and neurological disorders, such as Alzheimer’s disease or Parkinson’s disease. Disruption of this fragile equilibrium is often associated with health degradation and ultimately, death. Cellular homeostasis plays a critical role in how an organism will develop and age. ![]()
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