Abstract
Zinc's roles in brain function are poorly understood. Zinc is essential preβ and postnatally for growth, maturation, and function. In early pregnancy, zinc is essential for cell multiplication and implantation of the embryo and for cell differentiation and organ formation. Deficiency causes teratology in all tissues. Zn deficiency in later pregnancy impairs neuronal replication and migration (as observed in cerebellar external granular cells). Synaptogenesis is impaired (as observed in Purkinje cells). It has been proposed that zinc deficiency impairs calcium channels causing a decrease in intracellular calcium that suppresses gene expression of growth factors and synthesis of nucleic acids and proteins. Whatever the mechanism, effects in experimental animals include poorly reversible impairments in learning and memory later in life, which appears associated with decreased neuronal survival. It is unknown if similar phenomena occur in humans. It is known however that low fetal growth, a process caused by maternal zinc deficiency, is risk factor for coronary heart disease, type 2 diabetes mellitus, chronic lung disease, and obesity. One wonders if fetal growth is related to later neuronal health and function. J. Trace Elem. Exp. Med. 16:165β173, 2003. Β© 2003 WileyβLiss, Inc.