A previous elegant work (performed in AD and DLB patients) corroborated this assumption, showing compensation through an increase in tyrosine hydroxylase (TH) mRNA expression in the remaining LC neurons, sprouting of dendrites into the peri-LC dendritic zone, and sprouting of axonal projections to the hippocampus as determined by alpha-2-receptor binding (Szot et al., 2006). This evidence concerns the gene TH and Alzheimer disease.