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OverviewFull Product DetailsAuthor: Lori M. BuhlmanPublisher: Springer International Publishing AG Imprint: Springer International Publishing AG Edition: 1st ed. 2016 Dimensions: Width: 15.50cm , Height: 1.80cm , Length: 23.50cm Weight: 5.561kg ISBN: 9783319421377ISBN 10: 3319421379 Pages: 275 Publication Date: 23 September 2016 Audience: Professional and scholarly , Professional & Vocational Format: Hardback Publisher's Status: Active Availability: Manufactured on demand ![]() We will order this item for you from a manufactured on demand supplier. Table of ContentsMitochondrial ROS and Apoptosis.- Dopamine Metabolism and Reactive Oxygen Species Production.- The Consequences of Damaged Mitochondrial DNA.- The role of chronic inflammation in the etiology of Parkinson’s disease.- Ion-Catalyzed Reactive Oxygen Species in Sporadic Models of Parkinson's Disease.- Toxin Mediated Complex I Inhibition and Parkinson’s Disease.- Parkinson Disease-Associated Mutations Affect Mitochondrial Function.- PARKIN/PINK1 Pathway for the Selective Isolation and Degradation of Impaired Mitochondria.- Mitochondrial Therapeutic approaches in Parkinson's Disease.- Altering Mitochondrial Fusion and Fission Protein Levels Rescues Parkin and PINK1 Loss-of-Function Phenotypes.- Early Nicotine Exposure is Protective in Familial and Idiopathic Models of Parkinson’s Disease.- Transcription Modulation of Mitochondrial Function and Related Pathways as a Therapeutic Opportunity in Parkinson’s Disease.- Delivery of Biologically Active Molecules to Mitochondria.ReviewsAuthor InformationLori Buhlman earned her Ph.D. in Neuroscience from the University of Arizona and trained as a post-doctoral fellow at the Institut National de la Santé et de la Recherche Médicale, in Paris, France. She is currently an associate professor of Biomedical Sciences and Behavioral Medicine at Midwestern University in Glendale, Arizona, where she manages a research program exploring the mechanisms by which loss of Parkin function causes neurodegeneration. Her recent publications report that nicotine can protect against motor deficits caused by Parkin loss of function in Drosophila, and that Parkin and PINK1 work together to promote mitochondrial homeostasis in a manner that involves mitochondrial fission protein, Drp1. Tab Content 6Author Website:Countries AvailableAll regions |