CHRONIC LOW-DOSE MPTP IN NONHUMAN-PRIMATES - A POSSIBLE MODEL FOR ATTENTION-DEFICIT DISORDER

Schneider and Kovelowski (1990) showed that chronic low-dose N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration to monkeys caused cognitive dysfunction without significant motor impairment on tasks thought to be related to the caudate-frontal axis. The cognitive difficulties were similar to those seen in monkey with frontal lesions, normal young monkeys, and normal young children. The caudate-frontal dysfunction is consistent with the cognitive difficulties that are thought to exist in children with attention deficit disorder (ADD). The caudate-frontal dysfunction is also consistent with the distribution of decreased cerebral blood flow and, presumably, decreased metabolism that has recently been found in children with ADD. In monkeys given chronic low-dose MPTP, pilot neurochemical studies have suggested abnormalities in dopamine and norepinephrine metabolism, the two neurotransmitters most frequently linked with ADD. We suggest that chronic low-dose MPTP induced cognitive dysfunction in primates may not only be a model for the cognitive disturbances that accompany Parkinson's disease but may also aid in understanding the cognitive dysfunction seen in children with ADD.