However, like anandamide, the other N-acylethanolamines (i.e. PEA and OEA), whose levels were shown to be elevated here in FTD mice, may also be elevated by FAAH inhibition, and produce neuroprotective actions by activating brain PPAR-α receptors (as in the case of OEA and PEA), or by desensitizing TRPV1 (as in the case of OEA and anandamide) and GPR55 (as in the case of PEA) receptors [14, 34]. The gene discussed is GPR55; the disease is frontotemporal dementia.