In other words, in AD, NEAT1 increases along with CDK5R1, indicating a peculiar functional relationship (in vitro defined as a negative NEAT1 control over CDK5R1) which is specific for AD and that can be either a protective response-related mechanism aimed at limiting (inefficiently) CDK5R1 upregulation or part of the disease pathogenesis. This evidence concerns the gene CDK5R1 and Alzheimer disease.