<?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%">Fang, E. F.</style></author><author><style face="normal" font="default" size="100%">Hou, Y.</style></author><author><style face="normal" font="default" size="100%">Palikaras, K.</style></author><author><style face="normal" font="default" size="100%">Adriaanse, B. A.</style></author><author><style face="normal" font="default" size="100%">Kerr, J. S.</style></author><author><style face="normal" font="default" size="100%">Yang, B.</style></author><author><style face="normal" font="default" size="100%">Lautrup, S.</style></author><author><style face="normal" font="default" size="100%">Hasan-Olive, M. M.</style></author><author><style face="normal" font="default" size="100%">Caponio, D.</style></author><author><style face="normal" font="default" size="100%">Dan, X.</style></author><author><style face="normal" font="default" size="100%">Rocktaschel, P.</style></author><author><style face="normal" font="default" size="100%">Croteau, D. L.</style></author><author><style face="normal" font="default" size="100%">Akbari, M.</style></author><author><style face="normal" font="default" size="100%">Greig, N. H.</style></author><author><style face="normal" font="default" size="100%">Fladby, T.</style></author><author><style face="normal" font="default" size="100%">Nilsen, H.</style></author><author><style face="normal" font="default" size="100%">Cader, M. Z.</style></author><author><style face="normal" font="default" size="100%">Mattson, M. P.</style></author><author><style face="normal" font="default" size="100%">Tavernarakis, N.</style></author><author><style face="normal" font="default" size="100%">Bohr, V. A.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Mitophagy inhibits amyloid-beta and tau pathology and reverses cognitive deficits in models of Alzheimer's disease</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Neurosci</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">*Mitophagy</style></keyword><keyword><style  face="normal" font="default" size="100%">Alzheimer Disease/*metabolism/pathology/psychology</style></keyword><keyword><style  face="normal" font="default" size="100%">Amyloid beta-Peptides/*metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals, Genetically Modified</style></keyword><keyword><style  face="normal" font="default" size="100%">Caenorhabditis elegans</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease Models, Animal</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hippocampus/*metabolism/*pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Induced Pluripotent Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Memory</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Neural Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Neurons/*metabolism/*pathology</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Mar</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">3</style></number><edition><style face="normal" font="default" size="100%">2019/02/12</style></edition><volume><style face="normal" font="default" size="100%">22</style></volume><pages><style face="normal" font="default" size="100%">401-412</style></pages><isbn><style face="normal" font="default" size="100%">1546-1726 (Electronic)1097-6256 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Accumulation of damaged mitochondria is a hallmark of aging and age-related neurodegeneration, including Alzheimer's disease (AD). The molecular mechanisms of impaired mitochondrial homeostasis in AD are being investigated. Here we provide evidence that mitophagy is impaired in the hippocampus of AD patients, in induced pluripotent stem cell-derived human AD neurons, and in animal AD models. In both amyloid-beta (Abeta) and tau Caenorhabditis elegans models of AD, mitophagy stimulation (through NAD(+) supplementation, urolithin A, and actinonin) reverses memory impairment through PINK-1 (PTEN-induced kinase-1)-, PDR-1 (Parkinson's disease-related-1; parkin)-, or DCT-1 (DAF-16/FOXO-controlled germline-tumor affecting-1)-dependent pathways. Mitophagy diminishes insoluble Abeta1-42 and Abeta1-40 and prevents cognitive impairment in an APP/PS1 mouse model through microglial phagocytosis of extracellular Abeta plaques and suppression of neuroinflammation. Mitophagy enhancement abolishes AD-related tau hyperphosphorylation in human neuronal cells and reverses memory impairment in transgenic tau nematodes and mice. Our findings suggest that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis and that mitophagy represents a potential therapeutic intervention.</style></abstract><accession-num><style face="normal" font="default" size="100%">30742114</style></accession-num><notes><style face="normal" font="default" size="100%">Fang, Evandro FHou, YujunPalikaras, KonstantinosAdriaanse, Bryan AKerr, Jesse SYang, BeimengLautrup, SofieHasan-Olive, Md MahdiCaponio, DomenicaDan, XiuliRocktaschel, PaulaCroteau, Deborah LAkbari, MansourGreig, Nigel HFladby, TormodNilsen, HildeCader, M ZameelMattson, Mark PTavernarakis, NektariosBohr, Vilhelm AengMC_PC_16034/MRC_/Medical Research Council/United KingdomZ01 AG000726-15/ImNIH/Intramural NIH HHS/Research Support, N.I.H., IntramuralResearch Support, Non-U.S. Gov'tNat Neurosci. 2019 Mar;22(3):401-412. doi: 10.1038/s41593-018-0332-9. Epub 2019 Feb 11.</style></notes><custom2><style face="normal" font="default" size="100%">PMC6693625</style></custom2><auth-address><style face="normal" font="default" size="100%">Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. e.f.fang@medisin.uio.no.Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lorenskog, Norway. e.f.fang@medisin.uio.no.Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Heraklion, Greece.Department of Basic Sciences, Faculty of Medicine, University of Crete, Heraklion, Greece.Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lorenskog, Norway.Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark.Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.Division of Medicine and Laboratory Sciences, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.Department of Neurology, Akershus University Hospital, Lorenskog, Norway.Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. bohrv@grc.nia.nih.gov.Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark. bohrv@grc.nia.nih.gov.</style></auth-address></record></records></xml>