<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Lou, G.</style></author><author><style face="normal" font="default" size="100%">Palikaras, K.</style></author><author><style face="normal" font="default" size="100%">Lautrup, S.</style></author><author><style face="normal" font="default" size="100%">Scheibye-Knudsen, M.</style></author><author><style face="normal" font="default" size="100%">Tavernarakis, N.</style></author><author><style face="normal" font="default" size="100%">Fang, E. F.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Mitophagy and Neuroprotection</style></title><secondary-title><style face="normal" font="default" size="100%">Trends Mol Med</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">*Ageing</style></keyword><keyword><style  face="normal" font="default" size="100%">*Alzheimer's disease</style></keyword><keyword><style  face="normal" font="default" size="100%">*amyotrophic lateral sclerosis</style></keyword><keyword><style  face="normal" font="default" size="100%">*energy homeostasis</style></keyword><keyword><style  face="normal" font="default" size="100%">*Mitochondria</style></keyword><keyword><style  face="normal" font="default" size="100%">*Mitophagy</style></keyword><keyword><style  face="normal" font="default" size="100%">*neurodegeneration</style></keyword><keyword><style  face="normal" font="default" size="100%">*Parkinson's disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Aging/physiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Homeostasis/physiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitochondria/physiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitophagy/*physiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Neurodegenerative Diseases/*physiopathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Neurons/physiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Neuroprotection/*physiology</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2020</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jan</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">1</style></number><edition><style face="normal" font="default" size="100%">2019/08/04</style></edition><volume><style face="normal" font="default" size="100%">26</style></volume><pages><style face="normal" font="default" size="100%">8-20</style></pages><isbn><style face="normal" font="default" size="100%">1471-499X (Electronic)1471-4914 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Neurodegenerative diseases are strongly age-related and currently cannot be cured, with a surge of patient numbers in the coming decades in view of the emerging worldwide ageing population, bringing healthcare and socioeconomic challenges. Effective therapies are urgently needed, and are dependent on new aetiological mechanisms. In neurons, efficient clearance of damaged mitochondria, through the highly evolutionary conserved cellular process termed mitophagy, plays a fundamental role in mitochondrial and metabolic homeostasis, energy supply, neuronal survival, and health. Conversely, defective mitophagy leads to accumulation of damaged mitochondria and cellular dysfunction, contributing to ageing and age-predisposed neurodegeneration. Here, we discuss the contribution of defective mitophagy in these diseases, and underlying molecular mechanisms, and highlight novel therapeutics based on new discovered mitophagy-inducing strategies.</style></abstract><accession-num><style face="normal" font="default" size="100%">31375365</style></accession-num><notes><style face="normal" font="default" size="100%">Lou, GuofengPalikaras, KonstantinosLautrup, SofieScheibye-Knudsen, MortenTavernarakis, NektariosFang, Evandro FengResearch Support, Non-U.S. Gov'tReviewEnglandTrends Mol Med. 2020 Jan;26(1):8-20. doi: 10.1016/j.molmed.2019.07.002. Epub 2019 Jul 30.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478 Lorenskog, Norway.Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Crete, Greece; Department of Basic Sciences, Faculty of Medicine, University of Crete, Heraklion, 70013, Crete, Greece.Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478 Lorenskog, Norway; The Norwegian Centre on Healthy Ageing (NO-Age), Oslo, Norway. Electronic address: e.f.fang@medisin.uio.no.</style></auth-address></record></records></xml>