Neuroprotective effects of antioxidants in the management of neurodegenerative disorders: A literature review

Panahi, Yunes; Rajaee, Seyyed Mahdi; Johnston, Thomas P.; Sahebkar, Amirhossein

doi:10.1002/jcb.26536

Cited by 27 publications

(21 citation statements)

References 83 publications

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“…In addition, current knowledge on treating schizophrenia with antioxidants is presented, along with information on how antioxidant levels in patients with schizophrenia may be regulated by nutritional, pharmacological, and lifestyle factors. Because schizophrenia is a progressive disorder from its onset in adolescence or early adulthood [ 10 , 26 , 27 , 28 ], the intake of natural antioxidants may help regulate its development [ 29 ].…”

Section: Introductionmentioning

confidence: 99%

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

Madireddy

2020

Brain Sciences

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The biochemical integrity of the brain is paramount to the function of the central nervous system, and oxidative stress is a key contributor to cerebral biochemical impairment. Oxidative stress, which occurs when an imbalance arises between the production of reactive oxygen species (ROS) and the efficacy of the antioxidant defense mechanism, is believed to play a role in the pathophysiology of various brain disorders. One such disorder, schizophrenia, not only causes lifelong disability but also induces severe emotional distress; however, because of its onset in early adolescence or adulthood and its progressive development, consuming natural antioxidant products may help regulate the pathogenesis of schizophrenia. Therefore, elucidating the functions of ROS and dietary antioxidants in the pathogenesis of schizophrenia could help formulate improved therapeutic strategies for its prevention and treatment. This review focuses specifically on the roles of ROS and oxidative damage in the pathophysiology of schizophrenia, as well as the effects of nutrition, antipsychotic use, cognitive therapies, and quality of life on patients with schizophrenia. By improving our understanding of the effects of various nutrients on schizophrenia, it may become possible to develop nutritional strategies and supplements to treat the disorder, alleviate its symptoms, and facilitate long-term recovery.

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Section: Introductionmentioning

confidence: 99%

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

Madireddy

2020

Brain Sciences

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“…Morato et al have shown that some phenolic compounds of olive oil (oleocanthals and triterpene acids) have strong neuroprotective effects and, therefore, can serve as a therapeutic intervention in the treatment of NDs. Additionally, they have reported that the Mediterranean diet, which is usually rich in olive oil, is associated with a lower incidence of NDs [80,81].…”

Section: Interventionsmentioning

confidence: 99%

“…Weinreb et al have documented that the polyphenolic components of green tea, with a high antioxidant capacity, can function as neuroprotective agent and reduce the incidence of DNs. Following this line of research, it is suggested that the consumption of green tea can protect neurons from oxidative stress damage [80].…”

Section: Interventionsmentioning

confidence: 99%

Frailty, Cognitive Decline, Neurodegenerative Diseases and Nutrition Interventions

Gómez-Gómez¹,

Zapico

2019

IJMS

138

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Currently the human population is aging faster. This leads to higher dependency rates and the transformation of health and social care to adapt to this aged population. Among the changes developed by this population is frailty. It is defined as a clinically detectable syndrome, related to the aging of multiple physiological systems, which prompts a situation of vulnerability. The etiology of frailty seems to be multifactorial and its pathophysiology is influenced by the interaction of numerous factors. Morley et al. propose four main mechanisms triggering the frailty: atherosclerosis, sarcopenia, cognitive deterioration and malnutrition, with their respective metabolic alterations. Malnutrition is associated with cognitive impairment or functional loss, but it is also known that an inadequate nutritional status predisposes to cognitive frailty. Additionally, nutritional factors that may influence vascular risk factors will potentially have an effect on dementia decline among patients with cognitive frailty. This review aims to describe the nutritional factors that have been researched so far which may lead to the development of frailty, and especially cognitive decline.

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“…Therefore, the study of paraquat in relation to Parkinson's disease is warranted [11]. The cellular mechanisms of protection against PQ toxicity include activation of antioxidant pathways and autophagy as well as overexpression of a heat shock proteins' machinery [12][13][14][15]. Thus, compounds that can trigger one or all of these strategies are of interest as cytoprotective agents.…”

Section: Introductionmentioning

confidence: 99%

Lanostane Triterpenoid Metabolites from a Penares sp. Marine Sponge Protect Neuro-2a Cells against Paraquat Neurotoxicity

et al. 2020

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The results of an investigation of the protective effects of five lanostane triterpenoids: 3β-acetoxy-7β,8β-epoxy-5α-lanost-24-en-30,9α-olide (1), 3β-hydroxy-7β,8β-epoxy-5α-lanost-24-en- 30,9α-olide (2), 29-nor-penasterone (3), penasterone (4), and acetylpenasterol (5), from a marine sponge, Penares sp., against paraquat-induced neuroblastoma Neuro-2a cell damage, are described. The influence of all compounds on viability of the Neuro-2a cells treated with paraquat (PQ) was studied with MTT and fluorescein diacetate assays as well as propidium iodide straining. 1,1-Diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity of the compounds as well as their influence on reactive oxygen species (ROS) level and mitochondrial membrane potential in PQ-treated neuronal cells were analyzed. Finally, the effect of the compounds on intracellular level of heat shock protein 70 kDa (Hsp70) and neurite outgrowth in PQ-treated Neuro-2a cells were studied. Studied triterpenoids demonstrated protective effects against PQ-induced neurotoxicity associated with the ability to reduce ROS intracellular level and diminish mitochondrial dysfunction. Acetylpenasterol (5), as a more promising neuroprotective compound, significantly increased the viability of Neuro-2a cells incubated with PQ as well as decreased intracellular ROS level in these cells. Moreover, acetylpenasterol induced Hsp70 expression in PQ-treated cells. It was also shown to inhibit PQ-induced neurite loss and recovered the number of neurite-bearing cells. The relationship between neuroprotective activity of the investigated compounds 1–5 and their chemical structure was also discussed.

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Neuroprotective effects of antioxidants in the management of neurodegenerative disorders: A literature review

Cited by 27 publications

References 83 publications

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

Regulation of Reactive Oxygen Species-Mediated Damage in the Pathogenesis of Schizophrenia

Frailty, Cognitive Decline, Neurodegenerative Diseases and Nutrition Interventions

Lanostane Triterpenoid Metabolites from a Penares sp. Marine Sponge Protect Neuro-2a Cells against Paraquat Neurotoxicity

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