Somatic mitochondrial DNA mutations do not increase neuronal vulnerability to MPTP in young POLG mutator mice.

[1]  T. Prolla,et al.  Accumulation of mitochondrial DNA deletions within dopaminergic neurons triggers neuroprotective mechanisms. , 2013, Brain : a journal of neurology.

[2]  T. Prolla,et al.  Behavioral and metabolic characterization of heterozygous and homozygous POLG mutator mice. , 2013, Mitochondrion.

[3]  Jessica M. Silvaggi,et al.  Pgc-1α Overexpression Downregulates Pitx3 and Increases Susceptibility to MPTP Toxicity Associated with Decreased Bdnf , 2012, PloS one.

[4]  M. Beal,et al.  Somatic mitochondrial DNA mutations in early parkinson and incidental lewy body disease , 2012, Annals of neurology.

[5]  Petteri Piepponen,et al.  Transgenic expression and activation of PGC-1α protect dopaminergic neurons in the MPTP mouse model of Parkinson’s disease , 2011, Cellular and Molecular Life Sciences.

[6]  Y. Kong,et al.  Increase in mitochondrial DNA mutations impairs retinal function and renders the retina vulnerable to injury , 2011, Aging cell.

[7]  Gregory C Kujoth,et al.  Endurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice , 2011, Proceedings of the National Academy of Sciences.

[8]  T. Prolla,et al.  Age‐dependent cardiomyopathy in mitochondrial mutator mice is attenuated by overexpression of catalase targeted to mitochondria , 2010, Aging cell.

[9]  Takuya Miyakawa,et al.  Mitochondrial DNA Mutations Induce Mitochondrial Dysfunction, Apoptosis and Sarcopenia in Skeletal Muscle of Mitochondrial DNA Mutator Mice , 2010, PloS one.

[10]  T. Prolla,et al.  Mitochondrial point mutations do not limit the natural lifespan of mice , 2007, Nature Genetics.

[11]  Jiandie D. Lin,et al.  Suppression of Reactive Oxygen Species and Neurodegeneration by the PGC-1 Transcriptional Coactivators , 2006, Cell.

[12]  Y. Mitsumoto,et al.  Age-related severity of dopaminergic neurodegeneration to MPTP neurotoxicity causes motor dysfunction in C57BL/6 mice , 2006, Neuroscience Letters.

[13]  C. Geula,et al.  Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons , 2006, Nature Genetics.

[14]  Robert W. Taylor,et al.  High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and Parkinson disease , 2006, Nature Genetics.

[15]  N. Wood,et al.  Expanding insights of mitochondrial dysfunction in Parkinson's disease , 2006, Nature Reviews Neuroscience.

[16]  T. D. Pugh,et al.  Mitochondrial DNA Mutations, Oxidative Stress, and Apoptosis in Mammalian Aging , 2005, Science.

[17]  Howard T. Jacobs,et al.  Premature ageing in mice expressing defective mitochondrial DNA polymerase , 2004, Nature.

[18]  D. D. Di Monte,et al.  Aging of the nigrostriatal system in the squirrel monkey , 2004, The Journal of comparative neurology.

[19]  G. Fiskum,et al.  Mitochondrial Mechanisms of Neural Cell Death and Neuroprotective Interventions in Parkinson's Disease , 2003, Annals of the New York Academy of Sciences.

[20]  J. Langston,et al.  The etiology of Parkinson's disease with emphasis on the MPTP story , 1996, Neurology.

[21]  Sangkot Marzuki,et al.  MITOCHONDRIAL DNA MUTATIONS AS AN IMPORTANT CONTRIBUTOR TO AGEING AND DEGENERATIVE DISEASES , 1989, The Lancet.

[22]  T. Ozawa,et al.  Hypothesis. Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases , 1989 .

[23]  J. Langston,et al.  Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis. , 1983, Science.