Fetal blood neurons

Experiments that reveal the effects of alcohol on nerve cells of the prenatal developing brain in humans are not feasible, but animal experiments show that exposure of the fetus to a relatively low level of ethyl alcohol in maternal and fetal blood promotes significant changes in the migration of neurons to... 

Methamphetamine passes the blood-brain barrier better than amphetamine, and there is evidence that chronic use of methamphetamine can result in permanent damage to dopamine neurons. Both pass the placental barrier, and there is some evidence that abuse by a pregnant woman can result in fetal abnormalities. Methamphetamine is found in breast milk. The half-life of methamphetamine and amphetamine is about 10 to 13 hours. Some methamphetamine is metabolized to amphetamine, and amphetamine-glucuronide can be detected in urine for about two days. About 50% of methamphetamine is excreted unchanged in the urine over two to three days. 

In spite of the increased activities of SOD-1 and GPx and normal catalase activity, increased lipid peroxides in the blood plasma of DS patients have been reported (K10), as has as an increased accumulation rate of age pigments (i.e., lipofuscin and ceroid, known products of lipid peroxidation) (K9). In addition, an early study showed increased lipid peroxides in the cerebral cortex of DS fetal brains (B15). More recently, cortical neurons from fetal DS and age-matched normal brains were shown to differentiate normally early in cell cultures. However, DS neurons subsequently degenerated and underwent apoptosis, whereas the normal cells remained viable (B18). In addition, the DS neurons exhibited a three- to fourfold increase in reactive oxygen species and increased lipid peroxidation that preceded cell death. Importantly, DS neuron degeneration could be prevented by treatment with the free radical spin trap A-ferf-butyl-2-sulphophenylnitrone, the... 

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