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Involved in the ongoing debate is the speculation that aluminum somehow affects neurofibrillary tangles. Initially, the scientific community believed that the high concentration of aluminum in NFTs was an irreparable event in a dying neuron¹. Presently, it is believed that aluminum plays a role in NFT formation by acting on the tau protein, the major component of NFTs.

Because tau contains multiple phosphorylation sites, aluminum acts as a catalyst for the nonenzymatic covalent shift of the triphosphate group from adenosine triphosphate (ATP) to tau. Aluminum, having a positive charge of three, bonds with three phosphates of ATP, each having a negative charge, because the triphosphates have a higher affinity for aluminum than the adenosine. From there, the phosphates, having a greater affinity for the tau protein than the aluminum, are transferred to the protein, causing its precipitation. When this occurs, the entire triphosphate group is transferred to the protein and results in the aggregation of tau².

Also, evidence of aluminum induced NFT formation in animals has been provided as support that aluminum does affect neurofibrillary tangles. In 1965, Klatzo and coworkers reported that the injections of aluminum salts in the brains of rabbits caused NFT formation³. Later, it was found that in cultured rat neurons, aluminum treatment prompts the formation of NFTs². In opposition, Lovell et al. argued that no significant differences in aluminum levels were found in "NFT-bearing neurons compared with NFT- free neurons" in AD patients⁴. In a study performed by M.P. Mattson and colleagues, data indicated that neuronal damage and an alteration of tau did not occur with increases in aluminum⁵. The data collected in this same study indicated that the collection of aluminum alone in neurons cannot perpetuate NFTs, the tell-tale features of Alzheimers disease⁵.