Student Research: Susan Leaman

, , 2002
Faculty Advisor: Terrance J. Kavanagh

Role of Negative Cell Cycle Regulators in Ethanol Inhibition of Astroglial Cell Proliferation


Abstract

In utero exposure of the fetus to alcohol may result in Fetal Alcohol Syndrome (FAS), the name given to a group of physical and behavioral defects that are the direct result of a woman's alcohol consumption during pregnancy. The principal features of FAS are central nervous system (CNS) dysfunction, growth deficiency, and particular facial features (Clarren and Smith, 1978; Streissguth et al. 1980). Effects of ethanol on the developing CNS are manifested in functional, physiological and cellular deficits evidenced by mental retardation, behavioral maladjustment, microencephaly, brain malformations, impaired cell proliferation and migration, and cell death. Reduced body weight, length, and microcephaly are evidence of long-term growth deficiencies associated with in utero ethanol exposure. The distinct facial characteristics of FAS are more arresting in early childhood and include a flat midface, a thin upper lip, and epicanthic fold among other craniofacial dysmorphology.

The severity of the injury to the fetus caused by alcohol is dependent on both the alcohol consumption patter, otherwise referred to as dose and duration, and the timing of alcohol consumption relative to the stage of fetal development. The timing issue includes critical windows of differential vulnerability among the various regions of the developing brain. Our understanding of the risk of FAS is based on the interplay between these two factors.

Taken from the beginning of thesis.