Dr Kim Tieu - ()
2013-present Principal Investigator, Associate Professor (Reader), Department of Clinical Neurobiology, Plymouth University Peninsula Schools of Medicine and Dentistry.
2013-present Adjunct Faculty, University of Rochester (Rochester, New York).
Qualifications & background 2004-2012 Principal Investigator ( Assistant Professor) Departments of Environmental Medicine and Neurology in the Center for Translational Neuromedicine, University of Rochester (Rochester, New York).
2004-2012 Principal Investigator ( Assistant Professor) Departments of Environmental Medicine and Neurology in the Center for Translational Neuromedicine, University of Rochester (Rochester, New York).
2000-2004 Post-doctoral fellow Department of Neurology, Columbia University, New York, New York.
1995-2000 Ph.D Neuroscience, Department of Neuropsychiatry, University of Saskatchewan, Canada.
1993-2000 Pharmacist Saskatchewan, Canada
1988-1993 B.S.P. Pharmacy, College of Pharmacy,
University of Saskatchewan, Canada.
My research interest has always been to study mechanisms of neuronal dysfunction and degeneration as seen in Parkinson’s disease (PD), with the ultimate goal of developing effective therapies for this devastating neurological disorder. Our research projects address the following fundamental questions: 1) Is mitochondrial dysfunction pathogenic in PD? If so, can mitochondrial dynamics be targeted for PD treatment? 2) Glial-neuronal interactions: How do glial cells contribute to the vulnerability of dopamine neurons (the primary cell type affected in PD)? 3) Gene-environment interactions: Do mutations linked to PD render dopamine neurons more susceptible to environmental insults? To address these questions, we perform rigorous biochemical, histological, functional and genetic analyses in experimental models of PD. When applicable, post-mortem human samples are also used.
UoP Research group membershipClinical Neuroscience
VOYAGE: Biomedical solutions
(2014) 'Cytosolic PINK1 escapes from mitochondria to promote dendritic outgrowth' J Neurochem 128 (6), pp 787 - 789 , DOI
(2013) 'Impaired mitochondrial dynamics and Nrf2 signaling contribute to compromised responses to oxidative stress in striatal cells expressing full-length mutant huntingtin' PLoS One 8 (3), p e57932 , DOI
(2012) 'Cultured astrocytes do not release adenosine during hypoxic conditions' J Cereb.Blood Flow Metab. 32 (1), pp e1 - e7 , DOI
(2012) 'Neuronal adenosine release, and not astrocytic ATP release, mediates feedback inhibition of excitatory activity' Proc.Natl.Acad.Sci U.S.A. 109 (16), pp 6265 - 6270 , DOI
(2012) 'PINK1-dependent recruitment of Parkin to mitochondria in mitophagy' Proc.Natl.Acad.Sci.U.S.A. 107 (1), pp 378 - 383 , DOI
(2011) 'A Guide to Neurotoxic Animal Models of Parkinson's Disease' Cold Spring Harbor Perspective in Medicine 1, p a009316
(2011) 'D-�-Hydroxybutyrate Is Protective in Mouse Models of Huntington's Disease' PLoS ONE 6(9): e24620. doi:10.1371/journal.pone.0024620,
(2011) 'Paraquat neurotoxicity is mediated by the dopamine transporter and organic cation transporter-3' Proc.Natl.Acad.Sci U.S.A. 108 (51), pp 20766 - 20771 , DOI
(2010) 'Adenosine A1 receptors mediate local anti-nociceptive effects of acupuncture' Nat.Neurosci. 13 (7), pp 883 - 888 , DOI
(2010) 'Astrocytes and therapeutics for Parkinson's disease' Neurotherapeutics. 7 (4), pp 413 - 423
(2010) 'Perturbations in mitochondrial dynamics induced by human mutant PINK1 can be rescued by the mitochondrial division inhibitor mdivi-1' J.Biol.Chem. 285 (15), pp 11740 - 11752 , DOI
(2009) 'The organic cation transporter-3 is a pivotal modulator of neurodegeneration in the nigrostriatal dopaminergic pathway' Proc.Natl.Acad.Sci.U.S.A. 106 (19), pp 8043 - 8048 , DOI
(2007) 'Silencing of the Pink1 gene expression by conditional RNAi does not induce dopaminergic neuron death in mice' international journal of biological sciences 3 (4), pp 242 - 50
(2005) 'Ablation of the inflammatory enzyme myeloperoxidase mitigates features of Parkinson's disease in mice' J.Neurosci. 25 (28), pp 6594 - 6600
(2005) 'Complex I deficiency primes Bax-dependent neuronal apoptosis through mitochondrial oxidative damage' Proc.Natl.Acad.Sci.U.S.A. 102 (52), pp 19126 - 19131
(2004) 'L-3-hydroxyacyl-CoA dehydrogenase II protects in a model of Parkinson's disease' Ann.Neurol. 56 (1), pp 51 - 60
(2003) 'D-beta-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson's disease' J.Clin.Invest. 112, pp 892 - 901
(2002) 'Blockade of microglial activation is neuroprotective in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson disease' J.Neurosci. 22 (5), pp 1763 - 1771
(2002) 'Resistance of alpha -synuclein null mice to the parkinsonian neurotoxin MPTP' Proc.Natl.Acad.Sci.USA 99 (22), pp 14524 - 14529
(2014) 'Mitochondrial Dynamics as a Potential Therapeutic Target for Parkinson’s Disease?' ADVANCES IN CLINICAL NEUROSCIENCE & REHABILITATION 14 (1), pp 6 - 8
(2006) 'Mitochondrial dysfunction and neurodegenerative disorders in the basal ganglia' in Bezard E (ed.) Recent Breakthroughs in Basal Ganglia Research New York: Nova Science Publishers