PEA is an analgesic with more proporties than most analgesics, it is a natural compound inhibiting pathological inflammation, such as in states characterized by slow inflammation and chronic low grade inflammation. Since the last 10 years more and more information has been gathered pointing out PEA is valuable in the inhibition of neuro-inflammatory states, including Alzheimer.
Recently it was stated that:
According with the neuroprotective profile of PEA observed during behavioral studies, experimental molecular and biochemical markers induced by Ab25-35 injection, such as lipid peroxidation, protein nytrosylation, inducible nitric oxide synthase induction, and caspase3 activation, were reduced by PEA treatment. These data disclose novel findings about the therapeutic potential of PEA, unrevealing a previously unknown therapeutic possibility to treat memory deficits associated with AD.
In Alzheimer around the plaques there is chronic inflammation, leading to tissue and brain destruction. Palmitoylethanolamide reduces the negative impact of the pathological effects if that inflammation in a model for Alzheimer’s disease.
Source:
Neuropsychopharmacology. 2012 Jun;37(7):1784-92. doi: 10.1038/npp.2012.25. Epub 2012 Mar 14.
Palmitoylethanolamide protects against the amyloid-β25-35-induced learning and memory impairment in mice, an experimental model of Alzheimer disease.
D’Agostino G, Russo R, Avagliano C, Cristiano C, Meli R, Calignano A.
