Hallmark lesions of Alzheimer's disease (AD) are filled with reactive immunocompetent microglia, suggesting that immunological aberrations may participate in the pathophysiology of this disorder. If immune-mediated processes are closely linked to neuronal breakdown it would be of importance to have a reliable means to detect these processes. Cerebrospinal fluid microglial antibodies found mainly in AD patients are discussed as such potential sources. These antibodies recognize microglia in the developing rat brain, in neuronal cultures and on AD cortical biopsies. Treatment aimed at downregulating microglial is discussed and may have therapeutic significance for AD patients. Largely this review presents current opinions which support the concept that inflammation and similar immune mechanisms need to be considered as participating in AD pathogenesis.