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Mohammed T. Abou-Saleh

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PRESENT AND FUTURE TREATMENTS OF AD 321‘‘superbly’’ on the Morris water maze, whereas untreated micedid not. The authors remarked that their data did not supportconcerns that attempts to remove b-amyloid from brain mightinadvertently cause wider dispersal and, therefore, moreextensive b-amyloid neurotoxic damage. A later populationbasedobservational study tested the hypothesis that the naturaloccurrence of antibodies to b-amyloid might reduce theincidence of dementia 102 . Although antibodies to b-amyloidcould be detected, no reduction in AD was found.CONCLUSIONThe future for AD therapy holds much promise. As the generalhealth of old people continues to improve and the incidence offunctional disabilities is reduced, so the achievement ofdementia prevention seems not only attainable but worthwhile.The huge collaborative international effort to understand themolecular pathology of AD and to design drugs to modifycritical steps is certain to bring great benefit to those at risk ofdementia.REFERENCES1. Porter R. The Greatest Benefit to Mankind: A Medical History ofHumanity from Antiquity to the Present. Fontana, 1997; 201–44.2. Whalley LJ. Early onset Alzheimer’s disease in Scotland: environmentaland familial factors. Br J Psychiat 2001; 178 (suppl.) s53–9.3. Rao VS, Cupples A, van Duijn CM et al. Evidence for major geneinheritance of Alzheimer’s disease in families of patients with andwithout apolipoprotein Ee4. Am J Hum Genet 1996; 59: 664–75.4. Cruts M, van Duyijn CM, Backhoven H et al. 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