Antioxidant Interventions in Neurodegenerative Disorders

Oxidative stress, characterised by an imbalance between the production of reactive oxygen species and the capacity of cellular antioxidant defences, is a convergent mechanism in the pathogenesis of Alzheimer’s disease, Parkinson’s disease and other age-related neurodegenerative disorders. Reactive oxygen species generated within mitochondria, at sites of neuroinflammation or during metal‐catalysed oxidation initiate lipid peroxidation, protein misfolding and DNA damage, thereby exacerbating neuronal dysfunction and death. Antioxidant interventions range from dietary modulation with vitamins and polyphenols to the development of mitochondria-targeted small molecules and nanoparticle delivery systems designed to cross the blood–brain barrier. Preclinical studies demonstrate that restoration of redox homeostasis can attenuate amyloid-β aggregation, reduce tau hyperphosphorylation, preserve synaptic integrity and enhance endogenous neurotrophic signalling. In human cohorts, higher intakes of dietary antioxidants correlate with slower cognitive decline, although clinical trials of single-agent therapies have produced mixed results. Emerging strategies are exploring combined regimens that couple antioxidants with anti-inflammatory or anti-amyloid drugs, precise targeting to vulnerable neuronal populations and early intervention in at-risk individuals. The global burden of neurodegenerative disease underscores the urgency of refining antioxidant approaches, optimising bioavailability and establishing standardised outcome measures to translate promising laboratory findings into effective preventive and therapeutic options.

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Antioxidant Interventions in Neurodegenerative Disorders publication trend

The graph below shows the total number of articles in antioxidant interventions in neurodegenerative disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Oxidative stress: An imbalance between the generation of reactive species and antioxidant defences, leading to cellular damage.

Reactive oxygen species (ROS): Highly reactive oxygen-containing molecules capable of oxidising lipids, proteins and nucleic acids.

Antioxidants: Molecules that neutralise reactive species, preventing or repairing oxidative damage.

Mitochondrial dysfunction: Impairment of mitochondrial function resulting in reduced energy production and elevated ROS generation.

Amyloid-β (Aβ): Peptide fragments prone to aggregation, forming extracellular plaques that disrupt neuronal communication in Alzheimer’s disease.

References

1. Real-time imaging of mitochondrial redox reveals increased mitochondrial oxidative stress associated with amyloid β aggregates in vivo in a mouse model of Alzheimer’s disease. Molecular Neurodegeneration (2024).
2. The role of composite dietary antioxidants in elderly cognitive function: insights from NHANES. Frontiers in Nutrition (2024).
3. Vitamin E and Its Molecular Effects in Experimental Models of Neurodegenerative Diseases. International Journal of Molecular Sciences (2023).