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Elevated levels of homocysteine (Hcy) and related metabolites are associated with Alzheimers disease (AD). Severe hyperhomocysteinemia causes neurological deficits and worsens behavioral and biochemical traits associated with AD. Although Hcy is precluded from entering the Genetic Code by proofreading mechanisms of aminoacyl-tRNA synthetases, and thus is a non-protein amino acid, it can be attached to proteins via an N-homocysteinylation reaction mediated by Hcy-thiolactone. Because N-homocysteinylation is detrimental to proteins function and biological integrity, Hcy-thiolactone detoxifying enzymes PON1, BLMH, BPHL have evolved. This review provides an account of the biological function of these enzymes and of consequences of their impairments leading to phenotypes characteristic of AD.
Hieronim Jakubowski (Wed,) studied this question.
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