Acute pain brings an alarm to the body of possible injuries and has normally a protective purpose. Conversely, chronic pain does not convey any useful information and has no biological benefit. Chronic pain is a major clinical problem that affects up to 30% of persons in the world. It includes neuropathic pain, caused by dysfunction, damage, or degeneration of the sensory nervous system.
It gives a feeling of general discomfort and lowers the quality of life. Medications, massage therapy, acupuncture, electrical stimulation, nerve blocks, and surgery are some traditional therapies for chronic pain: all unsatisfactory.
Hence, in this article, we will discuss how can Palmitoylethanolamide can help deal with this issue of Chronic pain and Neurogenerative Disease. So, become getting into Palmitoylethanolamide (PEA) at https://www.cofttek.com/product/544-31-0/ let us see what PEA is all about.
Palmitoylethanolamide (PEA) is both a naturally occurring lipid ingredient contained in foods/dietary supplements and an endogenous lipid mediator belonging to the class of fatty acid ethanol amides.
Evidence indicates that PEA is an important anti-inflammatory, analgesic, and neuroprotective mediator acting on several molecular targets in both central and peripheral organs and systems.
THE EFFECT OF PALMITOYLETHANOLAMIDE ON NEUROGENERATIVE DISEASES:
- Neurodegeneration, such as that observed in Alzheimer’s and Parkinson’s diseases (AD and PD) and multiple and amyotrophic lateral sclerosis (MS and ALS), consists of a gradual neuronal cell death affecting a specific cellular population of the CNS causing a progressive disability such as cognitive impairments, behavioral and motor dysfunctions up to paralysis. PEA has demonstrated to play a neuroprotective role in several experimental models of neurodegenerative diseases.
- In an animal model of Parkinson’s disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) the chronic treatment with PEA counteracted behavioral impairments, motor dysfunction, the loss of nigrostriatal neurons, astrocytes activation, altered expression of iNOS and microtubule-associated proteins.
- The treatment with PEA also restored the cognitive behavior and the altered expression of microtubule-associated protein (MAP-2) in a PPARα-dependent way. The co-PEA/ luteolin composite was also effective in reversing the altered expression of iNOS, GFAP, and brain-derived neurotrophic factor (BDNF) expression in hippocampal slice culture exposed to Aβ1-42 peptide.
- Thus, the neuroprotective effect of PEA is based on its capability to revert the altered expression of proteins strictly associated with AD or PD and to down-regulated the activation of pro-inflammatory/pro-apoptotic factors leading to neural loss. Thus, PEA seems to enhance or compensate endogenous defense mechanisms counteracting neuroinflammation and neurodegeneration development.
CONCLUSION AND SUMMARY:
The capability of PEA to modulate protective response in inflammatory, neurodegenerative, and chronic pain conditions suggests that endogenous PEA may be a component of the homeostatic system involved in the resolution program of neuroinflammation.
Consequently, the administration of exogenous PEA like Pterostilbene or the inhibition of PEA degradation may be a therapeutic strategy to counteract the neuroinflammation at the base of several neurological disorders.Read More