Molecular aspects of inflammatory and immune responses in Alzheimer'sdisease


R.N. Kalaria
Bok Engelsk 1996
Utgitt
1996
Omfang
Side 687- 693
Opplysninger
Recent advances indicate numerous molecular and cellular elements ofthe immune system are involved in the pathogenesis of Alzheimer'sdisease. Amyloid beta protein deposition induces many moleculesassociated with a predominantly local inflammatory response withinthe brain parenchyma. These responses also provoke the release ofimmune system mediators including cytokines, which all seem largelyto be produced by reactive cells such as astrocytes and microglia.Classical acute phase proteins of the pentraxin and serine proteaseinhibitor (serpin) families as well as a host of complement proteinsand some coagulation factors seem the most intrinsically involved.These secreted molecules display variable binding with theamyloidotic lesions. Although our understanding of the molecularspecificity and significance of the interaction of these proteinswithin the lesions is not replete, the development of uniqueinhibitors of the inflammatory reactions could provide therapeuticstrategies to impede the pathogenetic process. Currently, thisappears a more viable option than to inhibit amyloid beta productionor modify amyloid beta precursor protein processing, an approachwhich seems more complex.
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