Abstract
Experimental allergic encephalomyelitis (EAE), a T-cell mediated autoimmune disease, is widely considered as an animal model of multiple sclerosis (MS). It is believed that breakdown of the blood brain barrier (BBB) reflects the initial mechanism in the induction of EAE. It has been reported that while neonatally pinealectomized Wistar rats develop extensive pathological changes and severe neurologic deficits upon induction of EAE with allogeneic spinal cord in adjuvant, adult rats pinealectomized at 6 weeks of age appeared resistant to the induction of EAE. These findings suggest that: (a) the pineal gland influences the expression of EAE and, by inference, the integrity of the BBB; and (b) there is an age-related window of susceptibility to the development of EAE possibly related to the level of maturation of the pineal gland and functional integrity of the BBB. This age-related susceptibility to the development of EAE in rats may be relevant to the timing of aquision of MS where a viral infection in childhood is thought to initiate the induction of autosensitization to myelin antigens. More specifically, it is suggested that the viral infection associated with the development of MS most likely is acquired in infancy prior to the establishment of the melatonin circadian rhythms between 3 and 9 months of age.