Under the titel ‘Neuroglial Roots of Neurodegenerative Diseases: Therapeutic Potential of Palmitoylethanolamide in Models of Alzheimer’s Disease’, professor pharmacology and pharmacotherapeutics Luca Steardo and colleague Caterina Scuderi discuss the profile and their fidings related to PEA and Alzheimer.
Their group already demonstrated that beta amyloid significantly blunts PPAR-alpha in astrocytes, suggesting the possibility that down-regulation of this receptor may represent one of the molecular mechanisms by which this peptide induces astrocyte activation and, probably, exerts its toxicity. Furthermore, they showed that PEA is able to reverse the down-regulation of PPAR-alpha induced by beta amyloid, thus inhibiting astrocyte activation and the over-expression of pro-inflammatory molecules and signals. (in their paper: Scuderi, C.; Esposito, G.; Blasio, A.; Valenza, M.; Arietti, P.; Steardo, L. Jr; Carnuccio, R.; De Filippis, D.; Petrosino, S.; Iuvone, T.; Di Marzo, V.; Steardo, L. Palmitoylethanolamide counteracts reactive astrogliosis induced by ␣-amyloid peptide. J. Cell. Mol. Med., 2011, 15(12), 2664-2674.)
In a new study, reported in 2013 they reported that PEA may enhance neuroprotection against beta amyloid-induced neurotoxicity by reducing astrocyte activation and the subsequent neuroinflammatory process, as well as by exerting a direct effect on neurons. They also presented evidence that the observed effects from PEA are strictly dependent on the activation of PPAR-alpha, one of the main targets of PEA. They states at the end of their paper:
Since PEA is well tolerated in humans, based on the current results it is possible to suggest this compound as a novel and promising tool to treat neurodegenerative processes associated to A␣ deposition.
Source: Neuroglial Roots of Neurodegenerative Diseases: Therapeutic Potential of Palmitoylethanolamide in Models Of Alzheimer’s Disease. by Scuderi C, Steardo L.
CNS Neurol Disord Drug Targets. 2013 Feb 4.