Because beta-amyloid accumulations are prominent in the brains of individuals with Alzheimer's disease (AD), scientists have sought treatments that would prevent the accumulation of beta-amyloid or remove it after it has accumulated. One approach is to immunize people against beta-amyloid through vaccination. Immunization would use the body's immune system to prevent the accumulation or promote the removal of beta-amyloid in the same way immunization for infectious agents such as tetanus, diphtheria, typhoid and polio prevents them from causing those illnesses. The vaccination concept is clear and well proven and there is some promising evidence from animal models of AD. However, developing a vaccine against beta-amyloid that is both safe and effective in humans is proving to be a substantial challenge.

In 1999, researchers reported that a vaccine called AN-1792 prevented formation of beta-amyloid plaques in young transgenic mice (mice genetically programmed to have specific characteristics) that develop many beta-amyloid plaques. They also found that when older mice with already formed beta-amyloid plaques were vaccinated with AN-1792, they had reductions in brain beta-amyloid. The next step was to determine whether reduction in beta-amyloid deposits improved "mouse memory" using standard models of memory in mice. The results were positive. Nevertheless, optimism was tempered by awareness that the mouse strain studied did not have neurofibrillary tangles. Many times studies in animal models do not generalize to human disease in terms of benefit, tolerability or both.

The first substantial trial of AN-1792 in humans resulted in symptoms of inflammation of the brain and spinal cord in enough patients that the study was stopped. The concept of vaccination against excessive accumulation of beta-amyloid remains promising and an aggressive research program on vaccination continues.

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