Parkinson’s disease (PD) is a progressive neurodegenerative disease in the elderly, and no cure or disease-modifying therapies exist. Several lines of evidence suggest that mitochondrial dysfunction and oxidative stress have a central role in the dopaminergic neurodegeneration of PD. In this context, mitochondria-targeted therapies that improve mitochondrial function may have great promise in the prevention and treatment of PD. In this review, we discuss the recent developments in mitochondria-targeted antioxidants and their potential beneficial effects as a therapy for ameliorating mitochondrial dysfunction in PD.

Parkinson’s disease (PD), the second most common neurodegenerative disease worldwide, often occurs in middle-aged and elderly individuals. A comprehensive search of recent published articles between 2012 and 2022 in PubMed, Web of Science, Elesvier, Wliey and Springer was carried out, focusing on original publications related to natural products against PD by restoring mitochondrial dysfunction.

Alpha-Synuclein misfolding and aggregation are linked to the Parkinson's disease pathology. In the unbound form, α-synuclein is a typical intrinsically disordered protein. It can adopt different conformations depending on the environmental modulators. Many environmental factors promote α-synuclein misfolding and aggregation. Structural variability of aggregated forms correlates with their effects in vivo.

Aggregation of alpha-synuclein (αS) into oligomers is critically involved in the pathogenesis of Parkinson’s disease (PD). Using confocal single-molecule fluorescence spectroscopy, we have studied the effects of 14 naturally-occurring polyphenolic compounds and black tea extract on αS oligomer formation.

The E46K is a point mutation in alpha-synuclein (alpha-syn) that causes familial Parkinsonism with Lewy body dementia. We have now generated a cell model of Parkinsonism/Parkinson's disease (PD) and demonstrated cell toxicity after expression of E46K in the differentiated PC12 cells.