The neuronal and immune memory systems as supervisors of neural plasticity and aging of the brain: from phenomenology to coding of information.

The ultimate goal of this report is to learn how to manipulate the level of memory T cells for more effective treatment of such neurological diseases as multiple sclerosis (MS), where certain T cell subsets recognize self-antigens as opposed to pathogen antigens, and Alzheimer's disease (AD). Brain lesions (electrolitically, by kainic acid, with AlCl, and with 6-OHDA); stimulations (electrical, magnetic, or pharmacological); or restoration of some neurological functions (thermoregulatory and behavioral) by fetal graft allotransplantations in bilaterally lesioned anterior hypothalamic area (AHA-immune regulation) and nucleus basalis magnocellularis (NBM-experimental AD) in our studies were designed to reproduce immune and cognitive deficits induced by lesions of these brain structures. To localize memory traces in the immune system and in the brain we used ethanol and drugs such as kainic acid and 6-OHDA, which have been used very effectively to produce temporary lesions in the brain. Rats showed no learning and memory ability as well as inhibition of immune reactions.