Immune diagnosis of a subset of Alzheimer's disease with preliminary implications for immunotherapy.

Based on remarkable similarities between the central nervous system and the immune system [e. g., both systems have memory cells, both appear to have identical receptors for dopamine, acetylcholine, enkephalins, endorphins, sharing of antigenic determinants on one or another CNS cell and one or another type of immunocyte cell, both systems communicate by soluble substances (e.g., neurotransmitters and lymphokines, respectively)], we have postulated that some forms of Alzheimer's disease are due not to CNS cell death but rather to excess suppression of the brain "B-cell equivalent". We found a pyrrolidone analog useful in stimulating lymphocyte B-cell mitogenesis and function in vitro; this agent subsequently proved dramatically effective in several patients with severe T cell dysfunction and severe recurrent viral infection due to excess T cell suppression. Its use (3-6 months) proved remarkedly effective in certain patients with Alzheimer's disease (frontal lobe cerebral atrophy on CAT scan, duration at least 2 years). A subset with certain immunological dysfunction responded dramatically both immunologically and clinically. In responders in in vitro studies, the defect was corrected in vitro in the presence of the pyrrolidone analog but not by various neuroleptics. Patients without the defect or with the defect but no in vitro correction by pyrrolidone analog agent did not respond clinically. A switch from pyrrolidone to placebo resulted in immunologic and clinical relapse in 2-4 months.