Antioxidants to reduce schizophrenia risk
30 September 2014
In an article published in Neuron, Kim Do and her group reveal that deficits related to schizophrenia can be corrected by protecting a specific group of vulnerable neurons from oxidative stress.
Prof. Kim Do’s lab from the Centre for Psychiatric Neurosciences (CNP) and member of the NCCR-Synapsy, in collaboration with Dr Patricio O’Donnell’s group from the University of Maryland in Baltimore have just made a major step forward in the understanding of schizophrenia. Their article stirred major interest in the scientific and medical communities.
The researchers used a developmental rodent model relevant for schizophrenia: neonatal rats that receive a small brain lesion to the ventral hippocampus. Lesioned animals go on to show some aspects of schizophrenia pathophysiology as adults including specific changes in parvalbumin interneurons (PVI) essential for cognitive activity, and apparently caused by oxidative stress. The PVI oxidation regulation system was not directly affected showing that oxidative stress can arise from several origins.
Presymptomatic treatment of neonatal rats with the antioxidant, N-acetyl-cysteine reversed the PVI changes and excitingly also corrected electrophysiological and behavioural abnormalities known to be caused by the neonatal lesion and significant to schizophrenia. It appears then that during brain development several events may induce specific neuronal oxidative stress leading to development of schizophrenia.
The results could bring a new treatment for schizophrenia. Antioxidant drugs given presymptomatically at early ages to people at risk may be able to prevent the emergence of the disorder.
Author : Anne-Muriel Brouet, EPFL
Jan-Harry Cabungcal,Danielle S. Counotte, Eastman M. Lewis, Hugo A. Tejeda, Patrick Piantadosi, Cameron Pollock, Gwendolyn G. Calhoon, Elyse M. Sullivan, Echo Presgraves, Jonathan Kil, L. Elliot Hong, Michel Cuenod, Kim Q. Do, Patricio O’Donnell;
Juvenile antioxidant treatment prevents adult deficits in a developmental model of schizophrenia.
Neuron 83(5):1073-1084, Sept 2014. doi:org/10.1016/j.neuron.2014.07.028 >