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Defects in their distribution or function trigger axonal degeneration prior to somal damage [23]

are the classical E3 ubiquitin ligases of PPAR (Fig

3i): Together with homocysteine, adenosine is the product of SAH hydrolysis by AHCY, and thus a substrate for the reverse reaction when other routes of adenosine metabolism are interrupted, causing an increase in SAH 62,63