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Following its physiological action, 1,25(OH)D is further catabolized by CYP24A1 into final metabolites such as calcitroic acid and 1,25(OH)D26,23 lactone, which are subsequently excreted in bile or urine [96, 102].(Fig

In our study, we found that the increased A plaques firstly appeared in the cortex and hippocampus of earlier 8-week ethanol exposed APP/PS1 mice (in both 2BC and IP paradigms), and no A plaque was found even after 10 weeks ethanol exposure in WT mice, suggesting that chronic ethanol exposure did not directly result in A plaques but accelerate the A deposition