The Brain of a Baby With DS

I thought this was interesting. It was just published in November. The link to the full text is below. It kind of goes along the lines of what was discussed several months ago (maybe a year or more by now) on the ES list of the brain of a baby with DS being normal or abnormal from the get-go.

Fetal Down Syndrome Brains Exhibit Aberrant Levels of Neurotransmitters Critical for Normal Brain Development

Nigel Whittle, MAppScia, Simone B. Sartori, PhDa, Mara Dierssen, MD, PhDb, Gert Lubec, MDc and Nicolas Singewald, PhDa BACKGROUND. In the immature developing fetal brain, amino acids (such as -aminobutyric acid, and taurine) and monoamines (serotonin, noradrenaline, and dopamine) act as developmental signals or regulators. In subjects with Down syndrome, dysfunctional brain development is evident from birth as reduction in brain weight, as well as volume reductions in specific brain regions, and an altered number of neurons, dendrites, and dendritic branching is observed. However, mechanisms that underlie the observed dysfunctional brain development in Down syndrome are not clear. OBJECTIVES. Because diverse amino acids and monoamines are critical for normal brain development, we wanted to determine whether dysfunctional brain development observed in subjects with Down syndrome is associated with altered brain amino acid and/or monoamine levels. DESIGN/METHODS. We quantified tissue concentrations of diverse amino acids, including -aminobutyric acid and taurine, and the monoamines serotonin, noradrenaline, and dopamine in the frontal cortex of fetal Down syndrome tissue at a gestational age of 20 weeks versus age-matched control aborted fetuses. RESULTS. Fetal Down syndrome brains showed reductions in the levels of serotonin, -aminobutyric acid, taurine, and dopamine in the frontal cortex. No alteration in the levels of arginine, aspartate, glutamine, glutamate, glycine, histidine, serine, or noradrenaline was observed. CONCLUSIONS. Serotonin, -aminobutyric acid, taurine, and dopamine are critical for the acquisition of brain morphologic features, neuronal and glia proliferation, and synapse formation. The detected reductions in the levels of these neurotransmitters may indicate potential mechanisms for the observed dysfunctional neuronal development in the Down syndrome fetal brain. http://pediatrics.aappublications.org/cgi/content/full/120/6/e1465