Brain-reactive antibodies (BRA) have recently been suggested to be the cause of neurofibrillar tangles and neuritic plaques in brain neurons of normal elderly and in much greater number, senile dementic humans. Since the degree of cognitive decline observed is correlated with the appearance of these abnormalities, it is possible that the cognitive impairment is also partially due to BRA. NZB mice develop high levels of BRA after a few months of age and also display a marked learning deficit in an active shock avoidance task. We therefore propose to more thoroughly evaluate their sensorimotor, learning, and memory abilities and correlate them with BRA levels. If NZB mice model senile dementia, their learning and memory deficits will far exceed their sensorimotor dysfunctions. Should this be the case, a model of senile dementia of the Alzheimer type will be available for the exploration of specific etiological, prophylactic, and therapeutic aspects of the disease.