Additionally, a marked reduction in synapsin levels was found in the hippocampus of ALS/FTD patients with the C9orf72 mutation, and evidence from in vitro and in vivo studies on C9orf72 mutant mice suggested an interaction between C9orf72 and synapsin, with a consequent reduction in synapsin levels at presynaptic terminals and decreased synaptic density in the hippocampus [61]. This evidence concerns the gene C9orf72 and frontotemporal dementia.