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Neuroprotection and acidosis induced by cortical spreading depression

Authors Kwong KK, Chan ST

Received 25 October 2016

Accepted for publication 26 October 2016

Published 12 December 2016 Volume 2016:12 Pages 3191—3194

DOI https://doi.org/10.2147/NDT.S125677

Checked for plagiarism Yes

Editor who approved publication: Dr Roger Pinder


Kenneth K Kwong, Suk-tak Chan
 
Department of Radiology, MGH/MIT/HMS Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Boston, MA, USA
 
We read with interest the article “Cortical spreading depression produces a neuroprotective effect activating mitochondrial uncoupling protein-5” published in Neuropsychiatr Dis Treat by Viggiano et al.1 The authors showed that cerebral spreading depression (CSD) triggered uncoupling protein-5 (UCP-5),1 which had been reported to exert a long-term effect upon neuron protection.2 The result is another piece in CSD literature on modifying gene expressions to provide neuroprotection to subsequent ischemic episodes.3,4 

Authors' reply
Giovanni Messina1,2
Emanuela Viggiano1,3
Vincenzo Monda1
Antonietta Messina1
Fiorenzo Moscatelli2
Anna Valenzano2
Domenico Tafuri4
Vincenzo De Luca5
Giuseppe Cibelli2
Marcellino Monda1
 
1Section of Human Physiology and Unit of Dietetic and Sport Medicine, Department of Experimental Medicine, Second University of Naples, Caserta, 2Department of Clinical and Experimental Medicine, University of Foggia, Foggia, 3Department of Medicine, University of Padua, Padua, 4Department of Motor Sciences and Wellness, University of Naples “Parthenope,” Napoli, Italy; 5Department of Psychiatry, University of Toronto, Toronto, ON, Canada
 
Thank you for the attention paid to our article entitled: “Cortical spreading depression produces a neuroprotective effect activating mitochondrial uncoupling protein-5”.1 We do agree that cerebral spreading depression (CSD)-induced acidosis is an intriguing aspect of the neuroprotection puzzle. It is well known that CSD is involved in the pathophysiology of migraine, cerebral ischemia, subarachnoid hemorrhage, and traumatic brain injury.2–7 
View the original paper by Viggiano and colleagues.

 

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