FAAH and frontotemporal dementia: We also showed that inhibiting FAAH with the subsequent potential elevation of the brain levels of endogenous endocannabinoids and endocannabinoid-like mediators (which together constitute the “endocannabinoidome”; [14]), and hence of the activity of their several neuroprotective and anti-inflammatory mediators, may represent a novel disease modifying therapy against TDP-43-induced neuropathology in FTD, serving to limit glial reactivity, preserve neuronal integrity and improve cognitive deficits.