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Abstract
Mitochondria are multifunctional organelles that participate in a wide range of metabolic processes, including energy production and biomolecule synthesis. The morphology and distribution of intracellular mitochondria change dynamically, reflecting a cell’s metabolic activity. Oxidative stress is defined as a mismatch between the body’s ability to neutralise and eliminate reactive oxygen and nitrogen species (ROS and RNS). A determination of mitochondria failure in increasing oxidative stress, as well as its implications in neurodegenerative illnesses and apoptosis, is a significant developmental process of focus in this review. The neuroprotective effects of bioactive compounds linked to neuronal regulation, as well as related neuronal development abnormalities, will be investigated. In conclusion, the study of secondary components and the use of mitochondrial features in the analysis of various neurodevelopmental diseases has enabled the development of a new class of mitochondrial-targeted pharmaceuticals capable of alleviating neurodegenerative disease states and enabling longevity and healthy ageing for the vast majority of people.
Highlights
Licensee MDPI, Basel, Switzerland.During rapid proliferation, the molecular mechanisms involved in cell growth require mitochondrial energy products made by aerobic glycolysis [1]
In addition to converting energy substrates into ATP, mitochondria are involved in the metabolism of reactive oxygen species (ROS), calcium homeostasis, and apoptosis [7]
Fatty acid oxidation is essential for Niemann-Pick disease type C (NPC) maintenance and proliferation in hippocampus neurogenesis, and lipogenesis is required for neuronal differentiation [44]
Summary
The application of novel imaging and molecular biology technologies to mitochondrial studies has revealed several surprising properties and functions of mitochondria in neuroplasticity, including (-) rapid movement within and between subcellular compartments [9]; (-) fission and fusion, which have been facilitated by two distinct protein complexes incorporating GTPase [10]; (-) response to electrical activity and stimulation of neurotransmitter and growth factor receptors [11]; (-) serve as signalling outposts for kinases, deacetylases, and other signal transduction enzymes [12]. The absence and/or presence of ROS/RNS imbalances limits the identification of relevant antioxidant components with beneficial effects In this context, the contribution of this project is to present an overview of oxidative stress processes and antioxidant therapy for neuroprotection to make them more accessible
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