ty of beta-amyloid proteins to stick to each other to form plaquesö (New Treatment 2004, 5). Researchers also found traces of Alzhemed in cerebrospinal fluid of the studyÆs population, suggesting that the drug overcomes the blood-brain barrier. Individuals in the study with mild-to-moderate AlzheimerÆs were treated with Alzhemed for three months. At the end of the testing period, researchers report that ôlevels of beta-amyloid protein circulating in the CSF were reduced after three months of treatment in the highest dose groupsö (New Treatment 2004, 5). Such results point to the fact that less amyloid formation occurs in the brain as a result of Alzhemed.
Many of the new drugs being tested to slow or halt the progression of AlzheimerÆs disease target a group of enzymes that are known as secretases. Secretase production leads to the formation of beta-amyloid. New drugs are designed to interfere with secretases in order to inhibit the formation of beta-amyloid. As one AlzheimerÆs drug researcher maintains, ôTargeting the production of A-beta and its aggregation is now a key strategy in the development of novel therapeutic agents for the treatment of ADö (New 2004, 34). Such a focus has led researchers to study the potential of cholesterol-lowering drugs, protease inhibitors, nicotinic drugs, and others for their impact on AlzheimerÆs
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