MARATTO

review · Antioxidants

Oxidative Stress and Antioxidants in Neurodegenerative Disorders

2023592 citationsOpen accessUniversity College Hospital, Ibadan

In plain language

Neurodegenerative disorders represent a significant public health concern, characterised by complex factors leading to neuronal degeneration. This review highlights oxidative stress, an imbalance between pro-oxidant species and antioxidant systems, as a crucial element in these conditions. Oxidative stress involves increased reactive oxygen and nitrogen species and reduced endogenous antioxidants. The article examines the general impact of oxidative stress on the central nervous system and its specific roles in the pathophysiology of Alzheimer's disease, Parkinson's disease, Amyotrophic Lateral Sclerosis, and Huntington's disease. It also explores potential therapeutic strategies to reverse or mitigate oxidative stress, aiming to halt pathological progression and achieve clinical benefits in these disorders.

Key takeaways

  • Neurodegenerative disorders are complex conditions marked by neuronal degeneration and loss.
  • Oxidative stress, an imbalance of reactive species and antioxidants, is a key factor in the pathophysiology of these diseases.
  • Oxidative stress specifically influences the progression of Alzheimer's, Parkinson's, Amyotrophic Lateral Sclerosis, and Huntington's diseases.
  • Therapeutic approaches that target oxidative stress may help slow the pathological progression of neurodegenerative disorders.

Why it matters

Neurodegenerative diseases like Alzheimer's and Parkinson's cause immense suffering. Understanding underlying mechanisms, such as oxidative stress, is vital for developing effective treatments. This research helps identify pathways for new therapies that could slow disease progression, offering hope for improved patient outcomes and addressing a major global health challenge.

Commercialisation angle

This review explores therapeutic strategies to reverse or mitigate oxidative stress in neurodegenerative disorders. This early-stage research could inform the development of novel drug targets or interventions for conditions such as Alzheimer's, Parkinson's, ALS, and Huntington's disease. Pharmaceutical companies and biotechnology firms might utilise this knowledge to develop new treatments aimed at slowing disease progression and enhancing patient quality of life.

AI-generated from the published abstract. Always read the original work before citing.

Abstract

Neurodegenerative disorders constitute a substantial proportion of neurological diseases with significant public health importance. The pathophysiology of neurodegenerative diseases is characterized by a complex interplay of various general and disease-specific factors that lead to the end point of neuronal degeneration and loss, and the eventual clinical manifestations. Oxidative stress is the result of an imbalance between pro-oxidant species and antioxidant systems, characterized by an elevation in the levels of reactive oxygen and reactive nitrogen species, and a reduction in the levels of endogenous antioxidants. Recent studies have increasingly highlighted oxidative stress and associated mitochondrial dysfunction to be important players in the pathophysiologic processes involved in neurodegenerative conditions. In this article, we review the current knowledge of the general effects of oxidative stress on the central nervous system, the different specific routes by which oxidative stress influences the pathophysiologic processes involved in Alzheimer's disease, Parkinson's disease, Amyotrophic Lateral Sclerosis and Huntington's disease, and how oxidative stress may be therapeutically reversed/mitigated in order to stall the pathological progression of these neurodegenerative disorders to bring about clinical benefits.

Research topics

  • Amyotrophic Lateral Sclerosis Research
  • Parkinson's Disease Mechanisms and Treatments
  • Genetic Neurodegenerative Diseases

Read the original research

This page summarises published work. The authoritative version sits with the publisher.

DOI: 10.3390/antiox12020517

Is something wrong with this record? Report it or request removal.

Discussion

Discuss this research

Have you built on this work, tried to replicate it, or seen it applied in practice? Share what you know. Verified researchers and MARATTO™ domain experts can open a discussion, and any member can reply. Contributions are reviewed before they appear.

No discussion yet. Open the first thread.