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By Hooper N.M. (ed.)

This article brings jointly the most suggestions of biochemistry, cellphone biology, and molecular biology which are getting used to enquire the molecular foundation of Alzheimer's affliction. It presents a precis of at present on hand healing brokers and customers for destiny medicines.

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11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 37 and late-onset cases, and among male and female relatives in successive generations. Neurology 38, 207–212. van Duijn, C. , Chandra, C. , Fratiglioni, L, Graves, A. , et al. (1991) Familial aggregation of Alzheimer’s disease and related disorders: a collaborative re-analysis of case control. studies. Int. J. Epidemiol. 20(suppl. 2), S13–S20. Yatham, L. , McHale, P. , and Kinsella, A. (1988) Down’s syndrome and its association with Alzheimer’s disease.

Go, P. C. , et al. (1998) Alpha-2-macroglobulin is genetically asociated with Alzheimer’s disease. Nature Genet. 19, 357–360. Primary Drug Therapies for AD 45 3 Advances in Methodology and Current Prospects for Primary Drug Therapies for Alzheimer’s Disease David S. Knopman 1. Introduction There has been gratifying progress in the development of drugs for Alzheimer’s disease (AD). Even though the current generation of medications, the cholinesterase inhibitors (CEIs), has produced only modest benefits, our concept of an “effective” therapy has matured considerably over this time.

Bronson, R. , Chen, D. , and Tonegawa, S. (1997) Skeketal and CNS deficits in presenilin-1 deficient mice. Cell 89, 629–639. 69. , Baumann, K. , and Yankner, B. A. (1997) Developmental regulation of presenilin-1 processing in the brain suggests a role in neuronal differentiation. J. Biol. Chem. 272, 14505–14508. 70. , Olivo, J. , et al. (1997) Cellular expression and proteolytic processing of presenilin proteins is developmentally regulated during neuronal differentiation. J. Neurochem. 69, 2432–2440.

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