Down Syndrome (DS) subjects develop Alzheimer disease (AD) histopathology before they develop dementia. We compared the resting and flash stimulated electroencephalogram (EEG) of nondemented adult DS and age-matched control subjects, in search of EEG abnormalities that might correlate with AD histopathology. DS subjects had increased absolute power in all the EEG bands, independent of cognition functions measured by the Mini Mental State Examination and Picture Absurdities Test scores. In the power spectrum of the resting EEG, we found a cognition-related increase in power at 4.5 and 8.8 Hz, indicative of a-slowing, as in AD patients. In the stimulated EEG, we found several cognition-related abnormalities, such as decreased responses to 12-Hz Stimulation and decreased integral of β- and γ-band responses, indicative of decreased responsiveness to photic stimulation, as in AD patients. Therefore, nondemented DS and AD patients share several cognition related EEG abnormalities which are probably due to AD histopathology.

The ion permeability of the membrane junctions between Chironomus salivary gland cells is strongly depressed by treatments that are generally known to inhibit energy metabolism. These treatments include prolonged coolhag at 6°-8°C, and exposure to dinitrophenol, cyanide, oligomycin, and Nethylmaleimide. IntraceUular injection of ATP appears to prevent depression of junctional permeability by dinitrophenol or to reverse it. Ouabain, azide, pchloromercuriphenylsulfonic acid, reserpine, and acetazolamide fail to depress junctional permeability. Thus the ion permeability of the junctional membranes appears to depend on energy provided by oxidative phosphorylation. Possible energy-linked processes for maintaining junctional permeability are discussed, including processes involving transport of permeability-modifying species such as Ca ++ .

No abstract