In the aging brain there is a loss of neurons compensated for by a proliferation of glial cells. Because of the increased B-type monoamine oxidase (MAO) activity present in the glia, dopaminergic and 'trace aminergic' modulation in the brain declines in senescence. The significant increase of the incidence of depression in the elderly, the age-dependent decline in male sexual vigor and the frequent appearance of parkinsonian symptoms in the latter decades of life might be attributed to a decrease of dopamine and 'trace amines' in the brain. The outlines of a drug strategy to counteract these biochemical lesions of aging by chronic administration of (-)deprenyl (Jumex, Eldepryl), a selective inhibitor of B-type MAO, which facilitates dopaminergic and 'trace-aminergic' activity in the brain, are forwarded. The restitution and long-term maintenance of full scale sexual activity in aged male rats continuously treated with (-)deprenyl and the clinical observation that this drug prolongs in a statistically significant manner, the duration of the Parkinson's disease support the view that (-)deprenyl may improve deteriorating functions due to dopamine deficiency in the aging brain.
