Both primary and secondary prevention trials require careful attention to safety. The agents selected for prevention studies are frequently referred to as ‘neuroprotective.’ A term used to differentiate agents expected to reduce cognitive decline rather than relief of symptoms. Preventive mechanisms aim at reducing amyloid plaque by altering metabolisms or protecting cells from amyloid toxicity. These mechanisms are mostly proposed based on laboratory and animal studies as few markers of biological mechanisms available in humans exist. Several classes of agents with encouraging results have been tested. These are clearly discussed below.
First of all, statins, the HMG-CoA reductase are known to impact greatly on cognition, dementia and Alzheimer’s disease by reducing cholesterol levels in the body of humans (Sparkset. al., 2008, p.418). Secondly, tramiprosate, a 3-amino-1-propanasulfonic acid initially developed as a pharmaceutical treatment was examined in a two phased study of 58 patients with mild to moderate Alzheimer’s disease over three months. Patients receiving tramiprosate experienced a reduction in Alzheimer’s. Neurochem later reported that tramiprosate would be used as a nutraceutical. Thirdly, immunotherapy initiated by using fibrils for the development of Alzheimer’s vaccine was addressed in Schenk’s 1999 report as an option for regressing amyloid plaque. There was evidence of a patient demonstrating clearance of Aβ trace deposits from their cortex, and a substantial microglial response. It was further concluded that displacement of Aβ, even when embedded in plaques, is possible in humans when immunotherapeutic techniques are used.
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