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Med Hypotheses. 2013 Apr;80(4):475-80. doi: 10.1016/j.mehy.2013.01.010. Epub 2013 Jan 31.

Insulin-like growth factor and the etiology of autism.

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1
Department of Biochemistry, Touro College of Osteopathic Medicine, 230 West 125th Street, New York, NY 10027, United States. gary.steinman@touro.edu

Abstract

The basic hypothesis for this study is that reduced peripartum level of insulin-like growth factor-1 (IGF) due to genetic, epigenetic, or environmental factors is a sentinel biomarker of increased probability of later development of autism. The central objective of the resultant proposed study described here is examining if a correlation exists between the serum level of IGF in the fetus/newborn and the probability of autism developing later in the child. Mechanisms possibly causing such a decrease are considered. This would define a prospective biomarker for and possible etiology of this disorder. Insulin-like growth factor-1 directly affects the rate at which oligodendrocytes promote myelination in the central nervous system, especially in the brain. Factors which reduce the production or availability of IGF could retard normal nerve programming in the fetus or neonate. Thus, it would be desirable to arrest the pathologic processes of autism in the early neonatal stage before irreversible nerve damage occurs.

PMID:
23375408
DOI:
10.1016/j.mehy.2013.01.010
[Indexed for MEDLINE]
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