Nobody but ATH has an almost physiological iron chelator not harming mitochondria. Now it looks like major apolipoprotein E's are quite good in protecting mitochondria but ApoE4 is not. The mechanism is similar to Friedreich's ataxia in which frataxin is not produced enough because of a gene defect.
Although 40–65% of AD patients have at least one copy of the ε4 allele, APOE4 is not a determinant of the disease. At least one-third of patients with AD are APOE4 negative and some APOE4 homozygotes never develop the disease. Yet those with two ε4 alleles have up to 20 times the risk of developing AD (Wikipedia).
Nobody but ATH has an almost physiological iron chelator not...
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