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Review
. 2021 Aug 3:2021:9971885.
doi: 10.1155/2021/9971885. eCollection 2021.

Redox Homeostasis and Prospects for Therapeutic Targeting in Neurodegenerative Disorders

Musbau Adewumi Akanji  1 , Damilare Emmanuel Rotimi  2   3 , Tobiloba Christiana Elebiyo  3 , Oluwakemi Josephine Awakan  2   3 , Oluyomi Stephen Adeyemi  2   3
Affiliations
Review

Redox Homeostasis and Prospects for Therapeutic Targeting in Neurodegenerative Disorders

Musbau Adewumi Akanji et al. Oxid Med Cell Longev. .

Abstract

Reactive species, such as those of oxygen, nitrogen, and sulfur, are considered part of normal cellular metabolism and play significant roles that can impact several signaling processes in ways that lead to either cellular sustenance, protection, or damage. Cellular redox processes involve a balance in the production of reactive species (RS) and their removal because redox imbalance may facilitate oxidative damage. Physiologically, redox homeostasis is essential for the maintenance of many cellular processes. RS may serve as signaling molecules or cause oxidative cellular damage depending on the delicate equilibrium between RS production and their efficient removal through the use of enzymatic or nonenzymatic cellular mechanisms. Moreover, accumulating evidence suggests that redox imbalance plays a significant role in the progression of several neurodegenerative diseases. For example, studies have shown that redox imbalance in the brain mediates neurodegeneration and alters normal cytoprotective responses to stress. Therefore, this review describes redox homeostasis in neurodegenerative diseases with a focus on Alzheimer's and Parkinson's disease. A clearer understanding of the redox-regulated processes in neurodegenerative disorders may afford opportunities for newer therapeutic strategies.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1
Generation of reactive oxygen species and reactive nitrogen species. H2O: water; O2: oxygen; O2·-: superoxide anion; H2O2: hydrogen peroxide; CAT: catalase; SOD: superoxide dismutase; ONOO−: peroxynitrite; GSH: reduced glutathione; GSSG: glutathione disulfide; Fe2+: ferrous iron; ·OH: hydroxyl radical; NOS: nitric oxide synthase; L-Arg: L-arginine; L-Cit: L-citrulline; NO·: nitric oxide radical; LOOH: lipid hydroperoxides; LOO·: lipid peroxy radical; α-TOH: α-tocopherol; α-TO·: α-tocopheroxyl radical.
Figure 2
Figure 2
The role of oxidative stress in the pathology of Parkinson's disease.
Figure 3
Figure 3
The role of oxidative stress in Alzheimer's disease.
Figure 4
Figure 4
Antioxidant intervention at the cellular and molecular levels in neurodegeneration.
Figure 5
Figure 5
Schematic diagram on the effects of antioxidant on neuronal damage.
See this image and copyright information in PMC

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