Targeting intracellular and extracellular alpha-synuclein as a therapeutic strategy in Parkinson's disease and other synucleinopathies

2012 ◽  
Vol 16 (4) ◽  
pp. 421-432 ◽  
Author(s):  
Kostas Vekrellis ◽  
Leonidas Stefanis
2018 ◽  
Vol 8 (4) ◽  
pp. 52 ◽  
Author(s):  
Manuel Menéndez-González ◽  
Huber Padilla-Zambrano ◽  
Cristina Tomás-Zapico ◽  
Benjamin García

2019 ◽  
Vol 20 (8) ◽  
pp. 1850 ◽  
Author(s):  
Rijan Bajracharya ◽  
Neil A. Youngson ◽  
J. William O. Ballard

Mitochondrial dysfunction has been demonstrated to play an important role in the pathogenesis of Parkinson’s disease (PD). The products of several PD-associated genes, including alpha-synuclein, parkin, pink1, protein deglycase DJ-1, and leucine rich repeat kinase 2, have important roles in mitochondrial biology. Thus, modifying mitochondrial function could be a potential therapeutic strategy for PD. Dietary management can alter mitochondrial function as shifts in dietary macronutrients and their ratios in food can alter mitochondrial energy metabolism, morphology and dynamics. Our studies have established that a low protein to carbohydrate (P:C) ratio can increase lifespan, motor ability and mitochondrial function in a parkin mutant Drosophila model of PD. In this review, we describe mitochondrial dysfunction in PD patients and models, and dietary macronutrient management strategies to reverse it. We focus on the effects of protein, carbohydrate, fatty acids, and their dietary ratios. In addition, we propose potential mechanisms that can improve mitochondrial function and thus reverse or delay the onset of PD.


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