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A similar argument surrounds the possible involvement of aluminum in the formation of senile plaques. The roles that beta-amyloid protein and aluminum play in this formation has been the subject of many studies. Kuroda and colleagues performed a study on this relationship and concluded that aluminum promoted the aggregation of synthetic beta-amyloid protein. Because the aggregation of beta-amyloid protein results in neurotoxicity, the elevated presence of aluminum in the brain accelerates the aggregation of beta-amyloid protein in the brain tissue, therefore, accelerating the development of senile plaques and AD (Kuroda et al. 3).

A differing idea relating aluminum to the protein has been presented by M. Clauberg and J.G. Joshi, who speculate that aluminum could have an effect on the production of beta-amyloid protein by suppressing the inhibitor domain, making the cell incapable of suspending the production of the protein when there is an excess amount in the cell. Without anything to hold its level of production within a normal range, the beta-amyloid protein accumulates and increases the rate at which senile plaques are formed (Clauberg and Joshi 1009). In opposition to both of these ideas are many scientists who have failed to find a considerable elevation in aluminum levels in senile plaques. A group led by H. Jacqmin and associates concurs with the conclusion that there is no reliable evidence for aluminum in senile plaques (Jacqmin et al. 48).