Indirect evidence for altered dopaminergic neurotransmission in very premature-born adults.

While animal models indicate altered brain dopaminergic neurotransmission after premature birth, corresponding evidence in humans is scarce due to missing molecular imaging studies. To overcome this limitation, we studied dopaminergic neurotransmission changes in human prematurity indirectly by evaluating the spatial co-localization of regional alterations in blood oxygenation fluctuations with the distribution of adult dopaminergic neurotransmission. The study cohort comprised 99 very premature-born (<32 weeks of gestation and/or birth weight below 1500 g) and 107 full-term born young adults, being assessed by resting-state functional MRI (rs-fMRI) and IQ testing.

Altered Gray Matter Cortical and Subcortical T1-Weighted/T2-Weighted Ratio in Premature-Born Adults.

Background: Microscopic studies in newborns and animal models indicate impaired myelination after premature birth, particularly for cortical myelination; however, it remains unclear whether such myelination impairments last into adulthood and, if so, are relevant for impaired cognitive performance. It has been suggested that the ratio of T1-weighted (T1w) and T2-weighted (T2w) magnetic resonance imaging signal intensity (T1w/T2w ratio) is a proxy for myelin content. We hypothesized altered gray matter (GM) T1w/T2w ratio in premature-born adults, which is associated with lower cognitive performance after premature birth.