Abstract
About 10 years ago, we implicated immune factors in the pathophysiology of Alzheimer disease (AD), the hypothesis being that AD may be an immunologically derived systemic disease, but clinical effects confined primarily to the brain. We originally hypothesized that an immune basis of the disease may involve faulty immune regulation and autoimmunity. As described here, the activation of immunoregulatory T-lymphocytes with CD8 phenotype may be important in the immunopathogenesis of the disease.
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