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Boyd Haley PhD explains the link between APOE-4 genotype and Alzheimer's Disease.
In 1997, APO-E4 was identified as a significant risk factor for early onset of Alzheimer’s with APO-E2 being identified as protective against AD. Several subsequent papers failed to clarify the reason. APO-E has 299 amino acids with different ratios of cysteine and arginine at position 112 and 158. APO-E2 has 2 cysteines, apo-E3 one cysteine and one arginine, and APO-E4 two arginines. As arginine, unlike cysteine, lacks the sulphydryl (SH) groups to potentially bind bivalent metals such as mercury, lead, copper or zinc, it would be logical to suspect the possibility of increased metal accumulation in those chronically exposed individuals who had not inherited APO-E2. Godfrey 2003 found there was a statistically significant increase in adverse effects in those patients having APO-E4/4 and APO-E 3/4 where those patients were chronically exposed mercury. Godrey went on to explain why this occurs:
According to Saunders, the underlying reason for the apo-E-associated differences in AD susceptibility remains a mystery. However, a logical biochemical explanation has been proposed by Pendergrass and Haley, based on the different amino-acid configurations of the three apo-E isomers and their potential relevance to mercury elimination. Only ε2 (with two cysteine -SH groups), and to a lesser extent ε3 (with one –SH group), are able to bind and remove mercury from the brain and cerebrospinal fluid. This would oppose accumulation of mercury which is reported to be causal for the unique brain lesions that typify the AD brain including neuro-fibrillary tangles.