Lipopigment, identifiable in the fluorescence microscope, is thought to be cellular debris partly derived from free-radical-induced peroxidation of cellular constituents. The volume of neuronal lipopigment has been positively correlated with advancing age, Alzheimer dementia, and the neuronal ceroidoses, while various changes in neuronal lipopigment have been reported in association with the chronic administration of dihydroergotoxine, ethanol, phenytoin, centrophenoxine, and chlorpromazine. An increase in the volume of neuronal lipopigment may indicate increased functional activity of the cell, impaired removal of pigment or anoxia. Chronic administration of agents which can be correlated with decreased neuronal lipopigment in animal models might protect neuronal function against any adverse effects associated with (but not necessarily resulting from) lipopigment accumulation in normal ageing, anoxia, or certain degenerative diseases. Long-term studies of the prophylactic use of such agents, or of drugs which neutralise free radicals, may be indicated. Other clinical applications of such drugs may include protection against the effects of free radicals formed during periods of oxygen deprivation.