Perspectives on the Molecular Mediators of Oxidative Stress and Antioxidant Strategies in the Context of Neuroprotection and Neurolongevity

Abstract

Molecules with at least one unpaired electron in their outermost shell are known as free radicals. Free radical molecules are produced either within our bodies or by external sources such as ozone, cigarette smoking, X-rays, industrial chemicals, and air pollution. Disruption of normal cellular homeostasis by redox signaling may result in cardiovascular, neurodegenerative diseases and cancer. Although ROS (reactive oxygen species) are formed in the GI tract, little is known about how they contribute to pathophysiology and disease etiology. When reactive oxygen species and antioxidants are in imbalance in our bodies, they can cause cell structure damage, neurodegenerative diseases, diabetes, hypercholesterolemia, atherosclerosis, cancer, cardiovascular diseases, metabolic disorders, and other obesity-related disorders, as well as protein misfolding, mitochondrial dysfunction, glial cell activation, and subsequent cellular apoptosis. Neuron cells are gradually destroyed in neurodegenerative diseases. The production of inappropriately aggregated proteins is strongly linked to oxidative stress. This review’s goal is to provide as much information as possible about the numerous neurodegenerative illnesses linked to oxidative stress. The possibilities of multimodal and neuroprotective therapy in human illness, using already accessible medications and demonstrating neuroprotective promise in animal models, are highlighted. Neuroprotection and neurolongevity may improve from the use of bioactive substances from medicinal herbs like Allium stadium, Celastrus paniculatus, and Centella asiatica. Many neuroprotective drugs’ possible role has been addressed. Preventing neuroinflammation has been demonstrated in several animal models.