In a variety of animal models, PEA seems to have some promise; researchers have been able to demonstrate relevant clinical efficacy in a variety of disorders, from multiple sclerosis to neuropathic pain.
In the mouse forced swimming test, palmitoylethanolamide was comparable to fluoxetine for depression. An Italian study published in 2011 found that PEA reduced the raised intraocular pressure of glaucoma. In a spinal trauma model, PEA reduced the resulting neurological deficit via the reduction of mast cell infiltration and activation. PEA in this model also reduced the activation of microglia and astrocytes. Its activity as an inhibitor of inflammation counteracts reactive astrogliosis induced by beta-amyloid peptide, in a model relevant for neurodegeneration, probably via the PPAR-α mechanism of action. In models of stroke and other CNS trauma, PEA exerted neuroprotective properties.