Palmitoylethanolamide (PEA) has been studied extensively for its anti-inflammatory, analgesic, antiepileptic and neuroprotective effects.
A quote from a paper on the neuroprotective effects of palmitoylethanolamide, tested in models for Alzheimer’s disease, models of so called Aβ neurotoxicity.
β-amyloid (Aβ) is the core of pathology in ALzheimer and this protein induces glial activation and promotes release of proinflammatory molecules that may self-perpetuate reactive gliosis and damage neurons, thus amplifying neuropathological lesions occurring in Alzheimer’s disease (AD). Using various cultures, the autors found that PEA has clear anti-inflammatory properties working via the PPARα mechanism, and their experiments revealed that PEA reduces reactive gliosis and subsequently induces a marked rebound neuroprotective effect on neurons.
1. PEA inhibits astroglial proliferation and reduces neuronal loss in mixed neuroglia co-cultures exposed to Aβ.
2. PEA decreases astrocyte activation in organotypic cultures of rat hippocampi and rescues neuronal CA3 damage caused by Aβ challenge.
Our data suggest that PEA is capable of profoundly reducing reactive astrogliosis and of guaranteeing neuronal protection in Aβ-induced neuroinflammatory and neurodegenerative events.
Scuderi C1, Valenza M, Stecca C, Esposito G, Carratù MR, Steardo L. Palmitoylethanolamide exerts neuroprotective effects in mixed neuroglial cultures and organotypic hippocampal slices via peroxisome proliferator-activated receptor-α. J Neuroinflammation. 2012 Mar 9;9:49. doi: 10.1186/1742-2094-9-21.