Tetrahydrobiopterin in antenatal brain hypoxia-ischemia-induced motor impairments and cerebral palsy. Redox Biol 2017 Oct;13:594-599
Date
08/15/2017Pubmed ID
28803128Pubmed Central ID
PMC5554922DOI
10.1016/j.redox.2017.08.002Scopus ID
2-s2.0-85027861384 (requires institutional sign-in at Scopus site) 23 CitationsAbstract
Antenatal brain hypoxia-ischemia, which occurs in cerebral palsy, is considered a significant cause of motor impairments in children. The mechanisms by which antenatal hypoxia-ischemia causes brain injury and motor deficits still need to be elucidated. Tetrahydrobiopterin is an important enzyme cofactor that is necessary to produce neurotransmitters and to maintain the redox status of the brain. A genetic deficiency of this cofactor from mutations of biosynthetic or recycling enzymes is a well-recognized factor in the development of childhood neurological disorders characterized by motor impairments, developmental delay, and encephalopathy. Experimental hypoxia-ischemia causes a decline in the availability of tetrahydrobiopterin in the immature brain. This decline coincides with the loss of brain function, suggesting this occurrence contributes to neuronal dysfunction and motor impairments. One possible mechanism linking tetrahydrobiopterin deficiency, hypoxia-ischemia, and neuronal injury is oxidative injury. Evidence of the central role of the developmental biology of tetrahydrobiopterin in response to hypoxic ischemic brain injury, especially the development of motor deficits, is discussed.
Author List
Vasquez-Vivar J, Shi Z, Luo K, Thirugnanam K, Tan SAuthors
Karthikeyan Thirugnanam PhD Postdoctoral Fellow in the Pediatrics department at Medical College of WisconsinJeannette M. Vasquez-Vivar PhD Professor in the Biophysics department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
Alcohol OxidoreductasesAnimals
Cerebral Palsy
GTP Cyclohydrolase
Humans
Hypoxia-Ischemia, Brain
Oxidoreductases
Phosphorus-Oxygen Lyases
