title: Modulation of mitochondrial dysfunction in neurodegenerative diseases via activation of nuclear factor erythroid-2-related factor 2 by food-derived compounds.
abstract: Oxidative stress and mitochondrial dysfunction are early events in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and amyotrophic lateral sclerosis (ALS). Mitochondria are important key players in cellular function based on mitochondrial energy production and their major role in cell physiology. Since neurons are highly depending on mitochondrial energy production due to their high energy demand and their reduced glycolytic capacity mitochondrial dysfunction has fatal consequences for neuronal function and survival. The transcription factor nuclear factor erythroid-2-related factor 2 (Nrf2) is the major regulator of cellular response to oxidative stress. Activation of Nrf2 induces the transcriptional regulation of antioxidant response element (ARE)-dependent expression of a battery of cytoprotective and antioxidant enzymes and proteins. Moreover, activation of Nrf2 protects mitochondria from dysfunction and promotes mitochondrial biogenesis. Therefore, the Nrf2/ARE pathway has become an attractive target for the prevention and treatment of oxidative stress-related neurodegenerative diseases. Small food-derived inducers of the Nrf2/ARE pathway including l-sulforaphane from broccoli and isoliquiritigenin from licorice displayed promising protection of mitochondrial function in models of oxidative stress and neurodegenerative diseases and represent a novel approach to prevent and treat aging-associated neurodegenerative diseases.
authors.affiliation: Department of Chemistry and Pharmacy, Molecular and Clinical Pharmacy, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Cauerstr. 4, Haus 6, 91058 Erlangen, Germany; Department of Chemistry and Pharmacy, Emil Fischer Center, Henriette Schmidt-Burkhardt Chair of Food Chemistry, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Schuhstr. 19, 91052 Erlangen, Germany. Electronic address: isabel.denzer@fau.de.
authors.forename: Isabel
authors.initials: I
authors.lastname: Denzer
authors.affiliation: Department of Pharmacology, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia; Centre for Complementary Medicine Research, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia; Molecular Medicine Research Group, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751,Australia. Electronic address: G.Muench@uws.edu.au.
authors.forename: Gerald
authors.initials: G
authors.lastname: Münch
authors.affiliation: Department of Chemistry and Pharmacy, Molecular and Clinical Pharmacy, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Cauerstr. 4, Haus 6, 91058 Erlangen, Germany. Electronic address: kristina.leuner@fau.de.
authors.forename: Kristina
authors.initials: K
authors.lastname: Friedland
mesh_terms: D000818:Animals; D005502:Food; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D051267:NF-E2-Related Factor 2 / Q000378:metabolism*; D019636:Neurodegenerative Diseases / Q000378:metabolism*; D018384:Oxidative Stress
chemical_list: D051267:NF-E2-Related Factor 2
keywords: Aging; Mitochondrial dysfunction; Nrf2; Nutrition; Oxidative stress