Based on the data showing a correlation between Semaphorins/Plxns and AD pathology, it would be interesting to investigate whether targeted overexpression of Semaphorins, such as Sema3A, or Plxns, such as PlxnA4 or PlxnB1, in the hippocampus or cortex of mice is sufficient to induce an AD-like phenotype. This evidence concerns the gene SEMA3A and Alzheimer disease.