Free radicals in Alzheimer’s disease

Rather scanty evidence exists for the participation of free radicals in Alzheimer s disease and Down s syndrome. However, more recendy, reports have appeared that suggest possible free-radical involvement in the pathogenesis of these two conditions. Zemlan et al. (1989) repotted that the activity of the free-radical scavenging enzyme, SOD, was significantly increased in fibroblast cell lines derived from familial Alzheimer s and Down s patients. They hypothesized that the elevation in SOD activity observed in the Alzheimer patients supports the theory that paired helical filaments are formed by free-radical hydroxylation of proline residues. They further su ested that SOD levels might also be increased in the brains of Alzheimer s and Down s patients, and that the increase in SOD may reflect an enhanced generation of free radicals. 

Despite the indications for involvement of free radicals in Alzheimer s disease and Down s syndrome pathogenesis summarized above, more evidence is needed to establish a role for free-radical mechanisms in these disease processes. If free radicals can be demonstrated to play a role in the pathogenesis of Alzheimer s disease and Down s syndrome, then this would set the stage for chronic therapy with antioxidants in these disease states. 

Retz, W., Gsell, W., Munch, G., Rosier, M., and Riederer, P. 1998. Free radicals in Alzheimer s disease. J. Neural. Transm. Suppl. 54, 221-236. 

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See also in sourсe #XX -- [ , ]

See also in sourсe #XX -- [ ]

See also in sourсe #XX -- [ ]

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