control samples is of special interest, despite the fact that the function of the amino acids deleted in this isoform has not been well documented. Conceivably, the alternative splicing factors that produce CNEX13-14 and 13-15 might be altered in AD brain. Alternatively, it may be that this relative preservation could indicate that the CNEX13-14 and 13-15 isoforms might be differentially expressed by cell types (e.g., microglia) whose abundance can be increased in AD brains. Understanding the functions of the individual PPP3CA isoforms and understanding the mechanisms whereby the differential splicing is regulated might each provide unique insights into specific AD pathogenetic features.
