Remarkably, only the treatment with BI rescued the respiration defects, both in PS‐DKO cells (Fig 1E and Appendix Fig S1S) and in FAD fibroblasts (Appendix Fig S1N), suggesting that increased levels of unprocessed C99, rather than the levels of Aβ, play a role in the mitochondrial dysfunction seen in AD. This evidence concerns the gene CACNA1A and Alzheimer disease.