Researchers are using their knowledge of the mechanisms underlying alcohol’s toxic effect on the fetus to design preclinical models that test the efficacy of a number of pharmaceutical agents to mitigate alcohol-related impairments (Idrus and Thomas 2011). For example, prenatal alcohol exposure results in deficient activation of cyclic-AMP response element–binding protein (CREB), which can impair brain plasticity, a process of neural change important for brain development, learning, and memory. The pharmaceutical vinpocetine, a vasodilator and anti-inflammatory agent, inhibits the enzyme phosphodiesterase type 1, an action that prolongs CREB activation and thereby strengthens synaptic connections. Studies in animal models find that vinpocetine attenuates alcohol-related impairments in cortical plasticity and reduces learning and memory deficits associated with developmental alcohol exposure (Medina 2011). Clinical trials in humans with dementia have shown some promise and no serious adverse consequences, although results with other disorders, such as ischemic stroke remain inconclusive (Medina 2011). Clinical studies to evaluate this drug in humans with FASD are an important next step.
