Abstract
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.
Highlights
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease in ageing individuals [1]
Aberrant mitochondrial forms and functions have been identified in a subset of patients with PD [6,7], which demonstrates that mitochondrial dysfunction and oxidative stress have a central role in PD pathogenesis
Improvement of mitochondrial function through dietary approaches is promoted for the management of diseases such as epilepsy, cancer, and diabetes
Summary
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease in ageing individuals [1]. Mitochondria are highly dynamic organelles which facilitate many cellular functions such as energy metabolism, the stress response, and cell death Considering their central role in cellular biochemistry it is not surprising that dysfunctional mitochondria can result in cellular damage and can be linked to a large variety of diseases (e.g., cancer, diabetes, epilepsy) and ageing. Various nutrition guides are published by medical and governmental institutions to educate the public [8,9] on what they should be eating to promote health and even prevent some diseases No such official guidelines have been formed to potentially delay the onset or slow the progression of PD. We note other models, including zebrafish (Danio rerio) [28,29] as well as non-human primate systems (e.g., reviewed in [30]) have been developed and have provided insight into PD
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