MOLECULAR ASPECTS OF INFLAMMATORY AND IMMUNE-RESPONSES IN ALZHEIMERS-DISEASE

Recent advances indicate numerous molecular and cellular elements of t he immune system are involved in the pathogenesis of Alzheimer's disea se. Amyloid beta protein deposition induces many molecules associated with a predominantly local inflammatory response within the brain pare nchyma. These responses also provoke the release of immune system medi ators including cytokines, which all seem largely to be produced by re active cells such as astrocytes and microglia. Classical acute phase p roteins of the pentraxin and serine protease inhibitor (serpin) famili es as well as a host of complement proteins and some coagulation facto rs seem the most intrinsically involved. These secreted molecules disp lay variable binding with the amyloidotic lesions. Although our unders tanding of the molecular specificity and significance of the interacti on of these proteins within the lesions is not replete, the developmen t of unique inhibitors of the inflammatory reactions could provide the rapeutic strategies to impede the pathogenetic process. Currently, thi s appears a more viable option than to inhibit amyloid beta production or modify amyloid beta precursor protein processing, an approach whic h seems more complex.