Specifically, we may define two high-degree sinks (Fig 3): CTNNB1 and JUN. Given these premises, we hypothesized that oxidative stress and DNA damage generated in response to energetic metabolism and Ca2+/K+ homeostasis impairments, could be among the major potential molecular underpinnings of FTD pathogenesis. This evidence concerns the gene CTNNB1 and frontotemporal dementia.