THE ROLE OF THE MAILLARD REACTION IN OTHER PATHOLOGIES - ALZHEIMERS-DISEASE

Many approaches have and are being undertaken to treat Alzheimer's dis ease but, as yet, no therapy is available with any established efficac y Given the heterogeneity of the aetiological factors involved in Alzh eimer's disease and the difficulties encountered in the clinical diagn osis, the lack of pharmacological success is not surprising. Furthermo re, the lack of an adequate animal model of Alzheimer's disease has de layed the development of novel therapeutic strategies. At present, and with the exception of the rarer forms of familial Alzheimer's disease , the need remains to treat the symptoms rather than the causes of the disease, primarily because the pathogenesis of Alzheimer's disease is still unknown. The evidence for the role of glycation and advanced gl ycation end-products (AGEs) in the formation of neurofibrillary tangle s and neuritic plaques, the characteristic histopathological lesions o f Alzheimer's disease, is briefly reviewed. While the role of glycatio n in the pathogenesis of Alzheimer's disease is not yet unequivocally proven, it is the only single protein modification that would explain the formation of both the characteristic histopathological lesions fir st described by Alois Alzheimer in 1907. With our improved understandi ng of the molecular basis for the clinical symptoms of dementia, it is hoped that the aetiological causes will afford more suitable targets for therapeutic intervention. In this respect it is interesting to not e that the anti-inflammatory compounds indomethacin and acetylsalicyli c acid, both inhibitors of the Maillard reaction, have been reported t o have therapeutic potential and the nootropic agent tenilsetam inhibi ts protein cross-linking by AGEs.