Abstract
Neurodegenerative diseases include a variety of pathologies such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and so forth, which share many common characteristics such as oxidative stress, glycation, abnormal protein deposition, inflammation, and progressive neuronal loss. The last century has witnessed significant research to identify mechanisms and risk factors contributing to the complex etiopathogenesis of neurodegenerative diseases, such as genetic, vascular/metabolic, and lifestyle-related factors, which often co-occur and interact with each other. Apart from several environmental or genetic factors, in recent years, much evidence hints that impairment in redox homeostasis is a common mechanism in different neurological diseases. However, from a pharmacological perspective, oxidative stress is a difficult target, and antioxidants, the only strategy used so far, have been ineffective or even provoked side effects. In this review, we report an analysis of the recent literature on the role of oxidative stress in Alzheimer’s and Parkinson’s diseases as well as in amyotrophic lateral sclerosis, retinal ganglion cells, and ataxia. Moreover, the contribution of stem cells has been widely explored, looking at their potential in neuronal differentiation and reporting findings on their application in fighting oxidative stress in different neurodegenerative diseases. In particular, the exposure to mesenchymal stem cells or their secretome can be considered as a promising therapeutic strategy to enhance antioxidant capacity and neurotrophin expression while inhibiting pro-inflammatory cytokine secretion, which are common aspects of neurodegenerative pathologies. Further studies are needed to identify a tailored approach for each neurodegenerative disease in order to design more effective stem cell therapeutic strategies to prevent a broad range of neurodegenerative disorders.
Highlights
Neurodegenerative diseases include a variety of pathologies such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and so forth, which share many common characteristics such as oxidative stress, glycation, abnormal protein deposition, inflammation, and progressive neuronal loss
Even ifif the the exact molecular mechanism causing dopaminergic cell death remains elusive, many studies observed exact molecular mechanism causing dopaminergic cell death remains elusive, many studies observed that the substantia nigra pars compacta of Parkinson’s disease (PD) patients is characterized by highly oxidized lipids, proteins, and DNA, together with low levels of glutathione [42]., Notably, in contrast to other regions of the brain, the substantia nigra is highly subjected to r9">9]. Oxidative stress can also (ROS) attack because neurons are exposed to additional oxidative stress due to their dopamine metabolism, low content of antioxidants, and high iron concentration [57]
Dopamine is oxidized by monoamine oxidases A and B with the production that the substantia nigra pars compacta of PD patients is characterized by highly oxidized lipids, proteins, and DNA, together with low levels of glutathione [42]., Notably, in contrast to other regions of the brain, the substantia nigra is highly subjected to ROS attack because neurons are exposed to additional oxidative stress due to their dopamine metabolism, low content of antioxidants, and high iron concentration [57]
Summary
Neurodegenerative diseases are a heterogeneous class of disorders characterized by a slow and chronic loss of different neuronal populations in the central nervous system (CNS). RNS are produced by the fast reaction of O2 with nitric oxide characterized by an elevated oxygen consumption, high levels of iron and copper, involved in ROS (NO), resulting in the generation of peroxynitrite (ONOO−) that can trigger DNA fragmentation and production, elevated content of polyunsaturated acids,namely and low antioxidant defenses [1,8]. Principally in the mitochondria, as they arebinding the largest oxygen enhances theare expression of generated these antioxidant enzymes thanks to its to a intracellular specific sequence in consumer during electron transfer in mitochondrial respiratory chain by the interaction between the promoter region of these genes called antioxidant response element (ARE) [15,16]. We describe the impact of oxidative stress in different neurodegenerative diseases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
