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In a cohort study of 38 children with congenital cataracts, a missense mutation in CYP51A1 was identified in one family [79]

We propose a mechanism to better explain the downstream pathophysiological events in AD powered by age-related intracellular aggregation of amyloid- (A) in the vesicular trafficking system initiated by an oxidative shift in redox state that lowers bioenergetic capacity [2, 3]