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Introduction: Individuals with Down syndrome (DS) exhibit Alzheimer's disease (AD) neuropathology and dementia early in life. Blood biomarkers of AD neuropathology would be valuable, as non-AD intellectual disabilities of DS and AD dementia overlap clinically. We hypothesized that elevations of amyloid beta (A beta) peptides and phosphorylated-tau in neuronal exosomes may document preclinical AD. Methods: AD neuropathogenic proteins A beta(1-42), P-T181-tau, and P-S396-tau were quantified by enzyme-linked immunosorbent assays in extracts of neuronal exosomes purified from blood of individuals with DS and age-matched controls. Results: Neuronal exosome levels of A beta(1-42), P-T181-tau, and P-S396-tau were significantly elevated in individuals with DS compared with age-matched controls at all ages beginning in childhood. No significant gender differences were observed. Discussion: These early increases in A beta(1-42), P-T181-tau, and P-S396-tau in individuals with DS may provide a basis for early intervention as targeted treatments become available. (C) 2016 Published by Elsevier Inc. on behalf of the Alzheimer's Association.

We examined clinical and neurophysiologic measures in 10 children 4 to 9 years after neonatal extracorporeal membrane oxygenation. Electroencephalograms did not correlate with clinical or other neurophysiologic measures of interhemispheric asymmetry. By ultrasound imaging, the right internal carotid artery velocity was approximately 62% of that on the left, and right internal cartoid flow was reduced by 74% (p≤0.01), whereas an age-matched control group showed no differences. A decrease in the amplitude of the long-lalency auditory and somatosensory evoked potentials was noted over the right hemisphere after left-sided stimulation compared with the left hemispheric potentials after right-sided stimulation (p≤0.005). No significant differences in hemispheric symmetry were noted in the amplitudes for wave V of the auditory brain-stern response or in the P30 component of the middle-latency auditory evoked potentials. Likewise, latency measures of the evoked potentials were symmetric. We conclude that (1) neonatal extracorporeal membrane oxygenation is associated with long-lasting decreased right internal carotid blood flow with compensatory increased flow through the left carotid system and (2) there is a consistent reduction in the amplitude of right hemispheric long-latency evoked potentials. These latter findings may reflect redirected cerebral blood flow patterns after extracorporeal membrane oxygenation. © 1990 The C.V. Mosby Company.