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PLoS One. 2012;7(8):e41880. doi: 10.1371/journal.pone.0041880. Epub 2012 Aug 17.
Neuroprotective activities of palmitoylethanolamide in an animal model of Parkinson's disease.
Esposito E1, Impellizzeri D, Mazzon E, Paterniti I, Cuzzocrea S.
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Abstract
The biochemical and cellular changes that occur following treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahyropyridine (MPTP) are remarkably similar to that seen in idiopathic Parkinson's disease (PD). PD is characterized by the degeneration of dopaminergic nigrostriatal neurons, which results in disabling motor disturbances. Activation of glial cells and the consequent neuroinflammatory response is increasingly recognized as a prominent neuropathological feature of PD. There is currently no effective disease-modifying therapy. Targeting the signaling pathways in glial cells responsible for neuroinflammation represents a promising new therapeutic approach designed to preserve remaining neurons in PD. Chronic treatment with palmitoylethanolamide (PEA, 10 mg/kg, i.p.), initiated 24 hr after MPTP injection (20 mg/kg), protected against MPTP-induced loss of tyrosine hydroxylase positive neurons in the substantia nigra pars compacta. Treatment with PEA reduced MPTP-induced microglial activation, the number of GFAP-positive astrocytes and S100β overexpression, and protected against the alterations of microtubule-associated protein 2a,b-, dopamine transporter-, nNOS- positive cells in the substantia nigra. Furthermore, chronic PEA reversed MPTP-associated motor deficits, as revealed by the analysis of forepaw step width and percentage of faults. Genetic ablation of peroxisome proliferator activated receptor (PPAR)-α in PPAR-αKO mice exacerbated MPTP systemic toxicity, while PEA-induced neuroprotection seemed be partially PPARα-dependent. The effects of PEA on molecules typically involved in apoptotic pathways were also analyzed. Our results indicate that PEA protects against MPTP-induced neurotoxicity and the ensuing functional deficits even when administered once the insult has been initiated.

PMID: 22912680 [PubMed - indexed for MEDLINE] PMCID: PMC3422290


Extra links:
http://www.ncbi.nlm.nih.gov/pubmed/24412329

http://www.ncbi.nlm.nih.gov/pubmed/24412329

(it is obvious PPAR alpha is not well understood in PD, though I remember a discussion topic about manipulating this pathway in PD at the WPC way back in 2004. I have not followed up on this potential therapy. I found a discussion of PurePEA, the supplement, utilized on another forum concerning mast cell stabilizers. Seems it is utilized as a prostaglandins inhibitor. )

Curr Med Chem. 2014;21(24):2803-21.
Neuroprotective properties of peroxisome proliferator-activated receptor alpha (PPARα) and its lipid ligands.
Fidaleo M, Fanelli F, Ceru MP, Moreno S1.
Author information
Abstract
Signalling lipids are known to control a wide array of cellular processes, including cell proliferation, apoptosis, migration, and energy metabolism. Fatty acids and their derivatives, eicosanoids, phosphoinositides, sphingolipids, some cannabinoid-like molecules bind and activate nuclear receptors, including peroxisome proliferator-activated receptors (PPARs). This subfamily of transcription factors comprises three isotypes - PPARα (NR1C1), PPAR β/δ (NR1C2), PPARγ (NR1C3) - which bind to specific DNA response elements, as heterodimers with retinoid X receptors. PPAR activity is modulated by post-translational modifications and cofactors, towards which they show differential affinity. The three PPARs mutually interact, being integrated in a complex system, leading to the concept of a "PPAR triad". Nevertheless, the isotypes also show distinct actions on cellular physiology and partially different tissue, ligand and target gene specificities. In the brain, while the functions of PPARγ and its ligands are being thoroughly investigated, the actual and potential roles of PPARα and β/δ are far from being clarified. PPARα appears especially intriguing, since it is selectively expressed in certain brain areas and neuronal/glial populations, and modulates antioxidant responses, neurotransmission, neuroinflammation, neurogenesis, and glial cell proliferation/differentiation. This receptor and its endogenous ligands, including oleoylethanoloamide (OEA) and palmitoylethanolamide (PEA), are involved in physiological and pathological responses, such as satiety, memory consolidation, and modulation of pain perception. The protective role of PPARα agonists in neurodegenerative diseases and in neuropsychiatric disorders makes manipulation of this pathway highly attractive as therapeutic strategy for neuropathological conditions. In this review, we focus on the pleiotropic functions of PPARα and its lipid ligands in the nervous tissue, devoting special attention to neuroprotection.

PMID: 24606520 [PubMed - indexed for MEDLINE]

PurePEA is manufactured in the Netherlands and can be found in protein powders in the US. I did find a link for purchasing this supplement in capsule form; seems it is used for many things in Europe(note the price is in Euros). I am just sharing information I uncover about potential alternative therapies--I am not suggesting anyone try this. My husband (who has PD) has not tried this. He just began a different supplement. I have not done enough investigation on PEA yet to have him trial this new supplement.

http://www.rs4supplements.com/en/peapure-capsules

Has anyone tried this substance? would greatly appreciate opinion aobut its use. thanks, madelyn

We have had many discussions about this item on PN forum.
You can search this topic there. Much controversy as the Netherlands doctor who may or may not be a fraud.
Search PN using "normast" also as a keyword. Many of the posts were about it before the name change to PeaPure.

My reservations are that it is not well absorbed without some form of chemical manipulation. And it is very expensive.
There is a patent for micronizing this powder to use sublingually, but then PeaPure says to use the regular capsules after the packets/sachets in the beginning. Which makes no sense to me.

There is one poster on RSD forum who used (uses) it for pain.
http://neurotalk.psychcentral.com/post1164839-33.html

When we were discussing this on PN I did search Google and found on some pain forums many said it did not work. A few liked it, but it wasn't a really positive impression that I had.