Zinc deficiency and neurodevelopment: The case of neurons

ANA M. ADAMO; PATRICIA I. OTEIZA

BIOFACTORS

IOS PRESS

Año: 2010 vol. 36 p. 117 - 124

0951-6433

Zinc is essential for normal brain development.   Gestational severe zinc deficiency can lead to overt fetal brain malformations.  Although not teratogenic, suboptimal zinc nutrition during gestation can have long-term effects on the offspring’s nervous system. This paper will review current knowledge on the role of zinc in modulating neurogenesis and neuronal apoptosis, as well as the proposed underlying mechanisms.  A decrease in neuronal zinc causes cell cycle arrest, which in part involves a deregulation of select signals (ERK1/2, p53, NF-êB).  Zinc deficiency also induces apoptotic neuronal death through the intrinsic (mitochondrial) pathway, which can be triggered by the activation of the zinc-regulated enzyme caspase-3, and as a consequence of abnormal regulation of pro-survival signals (ERK1/2, NF-êB).  Alterations in the finely-tuned processes of neurogenesis, neuronal migration, differentiation and apoptosis, that involve the developmental shaping of the nervous system, could have a long-term impact on brain health.  Zinc deficiency during gestation, even at the marginal levels observed in human populations, could increase the risk for behavioral/neurological disorders in infancy, adolescence and adulthood.