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6.16. THE LOCAL AMYLOIDOSIS IN GENERAL PARESIS, AS IN ALZHEIMER'S DISEASE, IS BETA AMYLOID


The immunocharacterization of the cortical amyloid depsits were analyzed in 8 patients with clinically, serologically and pathologically confirmed general paresis with slowly progressive dementia (atrophic form of dementia paralytica). A panel of antibodies recognizing various epitopes of the Aβ peptide, showed that the amyloid deposits correspond to Aβ.


Miklossy J, Rosemberg S, McGeer PL. Beta amyloid deposition in the atrophic form of general paresis. In: Alzheimer’s Disease: New advances. Eds: Iqbal K, Winblad B, J Avila. Medimond. Intyernational Proceedings. Proceedings of the 10th International Congress on Alzheimer’s Disease (ICAD) 2006; pp. 429-433.

 
Summary

Beta amyloid deposition is the main pathological feature of Alzheimer’s disease (AD). Dementia, cortical atrophy and amyloid deposits are also pathological features in the atrophic form of general paresis, a chronic bacterial infection, caused by the spirochete Treponema pallidum. In order to analyze whether the amyloid deposits in the atrophic form of general paresis may correspond to beta amyloid the brains of 7 patients who died with clinically and pathologically confirmed general paresis associated with slowly progressive dementia were analyzed. Bosma Steiner microwave technique was used to detect spirochetes and a panel of antibodies to detect beta amyloid. The results showed beta amyloid deposits in spirochetal colonies disseminated along the cerebral cortex and, in some cases, in the walls of cortical and leptomeningeal vessels. The results indicate that amyloid deposits in general paresis, as in AD, consist of beta amyloid. This should be included in our current concept of the pathogenesis of AD.