Disruption to higher order processes in Friedreich ataxia

doi:10.1016/j.neuropsychologia.2009.09.009
Received 1 April 2009; revised 21 July 2009; accepted 11 September 2009. 

Available online 17 September 2009.

Joanne Fielding^{a, b, c,}, Louise Corben^{d, e}, Phillip Cremer^f, Lynette Millist^c, Owen White^{b, c} and Martin Delatycki^{d, g}

^aCentre for Neuroscience, University of Melbourne, Parkville, Victoria, Australia
^bCentre for Developmental Psychiatry and Psychology, School of Psychology, Psychiatry, and Psychological Medicine, Monash University, Clayton, Victoria, Australia
^cDepartment of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australia
^dBruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Victoria, Australia
^eExperimental Neuropsychology Research Unit, School of Psychology, Psychiatry, and Psychological Medicine, Monash University, Clayton, Victoria, Australia
^fRoyal North Shore Hospital, N.S.W., Australia
^gDepartment of Paediatrics, University of Melbourne, Victoria, Australia

 Keywords: Friedreich ataxia (FRDA); cognition; saccades; cerebellum  

Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival

Journal of Neural Transmission,

Makoto Naoi1 , Wakako Maruyama2, Hong Yi1, Keiko Inaba1, Yukihiro Akao1, 3 and Masayo Shamoto-Nagai2


(1) Department of Neurosciences, Gifu International Institute of Biotechnology, 1-1 Nakafudogaoka, Kakamigahara Gifu, 504-0838, Japan

(2) Department of Geriatric Medicine, National Institute for Geriatrics and Gerontology, Obu, Aichi, Japan

(3) United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, Gifu, Japan

Received: 4 March 2009 Accepted: 30 August 2009 Published online: 18 September 2009

Keywords:  Apoptosis - Mitochondria - Oxidative stress - Redox state - Neuroprotection - MAO inhibitor