Other chapters in this issue discuss the evidence that implicates infection during infancy and childhood in the aetiology of respiratory disease. Here I argue that experience of infection in early life may also be involved in the aetiology of some diseases of the adult nervous system. The descriptive epidemiology of three neurological diseases is compatible with the hypothesis that they are delayed consequences of childhood infection. It is not difficult to imagine that the effects of an infection which results in loss of cells from an organ system, like the central nervous system, whose cell populations have lost the capacity to replace themselves by mitotic division could remain hidden until unmasked by ageing. Such a mechanism may be important in the aetiology of motor neuron disease and Parkinson′s disease. Age-related differences in host response, which may be partly related to a maturing immune system, are known to influence both short-and longterm outcome for several infections. Perhaps the immune response to infection with Epstein–Barr virus, or another common micro-organism with similar epidemiology, in adolescence or early adult life is sometimes directed at antigens that are also present in the central nervous system. At present, the evidence that supports these hypotheses is largely circumstantial. But it may possible to devise ways of testing them both epidemiologically and in the laboratory.