Parkinson’s disease is still difficult to treat. There are substances that supplement the lack of dopamine in the brain. However these do not treat the actual problem – degeneration of nerve cells in a part of the brain.
For a few years now a new chapter has been opened with knowledge that has been obtained about the natural repair mechanisms of our body. These substances responsible for repair and protection are a part of the group of body’s own molecules. One of those substances is called palmitoylethanolamide. A 2014 study showed that 30 Parkinson patients benefited from a yearlong treatment with palmitoylethanolamide.
A breakthrough was reported in 2012 when it turned out that palmitoylethanolamide can protect the nerve cells in the brain with Parkinson disease.
Palmitoylethanolamide (we will call it PEA) can be a valuable addition to the treatment of Parkinson’s disease. Below we will explain why.
PEA is a supplement with nearly no side effects and it is easy to use and can be used in combination with other Parkinson medication. On YouTube you can see a number of Parkinson patients that were happy with the results of smoking weed. However, Cannabis is not an option if you don’t want to feel stoned. PEA works in a similar way, only it does not make you stoned. That is why we are examining this substance here.
Parkinson’s disease: inflammation in the nervous system
There is hope again for Parkinson patients in the form of a body’s own, natural substance called palmitoylethanolamide.
A lot of promising results were announced in 2014 after 30 patients with severe Parkinson’s disease were treated with this substance, on top of their dopamine preparations, for a year.
The importance of researching new ways
In the scientific journal TRENDS in pharmacological sciences (2007 Vol.28 No.4), researchers and neurologists of several Italian universities and the ‘European Centre for Brain Research (CERC)’ describe the importance of a different approach to Parkinson’s disease.
They emphasize that neurobiological research in the last years clarified that Parkinson’s disease is connected to a chronic inflammation in the nervous system. This specifically shows from the presence of activated inflammatory cells close to the nerve cells in the substantia nigra that have been affected by Parkinson’s disease. These activated inflammatory cells destroy the still present and functioning nerve cells that produce dopamine.
We see the same thing in animal models of Parkinson’s disease. Here the dopamine producing nerve cells also degenerate and researchers see a lot of activated inflammatory cells. Furthermore it shows that with certain patients the severity of the disease is closely related to the activity of the inflammatory cells and inflammatory molecules.
Experiments show that a protective effect in the dopamine producing cells goes together with a decrease of activated inflammatory cells.
Researchers describes it as follows:
“More recently, the importance of neuroinflammation in PD pathophysiology has also emerged. Indeed, activated microglia have been described in close proximity to degenerating dopamine neurons in individuals with PD, and activation of microglia into the substantia nigra has been shown to cause selective destruction of dopamine neurons.
Furthermore, experimental parkinsonism, induced by neurotoxins specific to dopamine neurons, is coupled with the activation of nigral and striatal microglia and with the production of proinflammatory molecules. In addition, models of Parkinson’s disease inhibition of microglia is neuroprotective.
As in Alzheimers disease, polymorphisms of some cytokines have been identified as risk factors for Parkinson whereas epidemiological studies have reported that chronic users of anti-inflammatory drugs have a decreased risk for Parkinson… This protective effect is paralleled by a concomitant reduction in the associated microglial response and moderate, transient increases in cytokine levels at the sites of neurodegeneration. Therefore, modulation of the neuroprotective effect of peripheral inflammation might be exploited for improving the treatment of Parkinson’s disease.”
This is why substances which inhibit this inflammatory response and protect the nervous system against further damage are so important. Our body produces substances like this as a natural healing mechanism. These are called endocannabinoids, palmitoylethanolamide being one of them. After 2012, endocannabinoids are considered a new possible treatment for Parkinson’s disease. 
Treating Parkinson’s disease with the help of the body’s own protection mechanism of endocannabinoids: palmitoylethanolamide
The authors emphasize in the article that the body’s own reparative and regenerative mechanism possesses molecules of the endocannabinoid class.
“…we recall that the release of endocannabinoids during neuronal injury might constitute a protective response….”
This idea, that endocannabinoids can be of importance in the treatment of Parkinson’s disease was also clearly voiced in the online journal “Brain Briefings.”
“A growing body of evidence also indicates that modifying endocannabinoid levels in the brain’s striatum may help people with Parkinson’s and Huntington’s diseases. The striatum integrates signals from other brain areas, such as the substantia nigra, a central region for movement control. Scientists believe that imbalances in brain cell activity in these pathways underlie the movement deficits of these diseases. Adjusting endocannabinoid levels may help restore balance.”
One of the most studied body’s own protective and regenerative substances is the endocannabinoid that goes by the name palmitoylethanolamide (PEA).
Meanwhile there has been a number of Parkinson patients who have experienced that taking this supplement contributes to better functioning and shape. Over a million patients have been treated with PEA in Europe and the substance has shown to be safe and easy to use in combination with other medicine.
Breakthrough 2012: Eposito’s conclusion
Based on an animal study, researchers concluded the following information:
“Our results indicate that the PEA is neuroprotective even when administered once the insult has been initiated. This point is of particular importance, as the lack of PD biomarkers and the difficulties of early diagnosis make the pharmacotherapy of PD possible only when dopamine neuronal loss is advanced and the first symptoms have appeared.
PEA, administered once the insult has been initiated, cuts off the link inflammation-gliosis-mitochondrial dysfunction and may be represent a good neurotropic support.
A comparison of PEA against minocycline, also known having neuroprotective activity, demonstrated superior recovery in the PEA-treated animals vs minocycline-treated mice. ”
Evaluation of PEA for Parkinson’s disease
A lot of research has been done on the safety and effectiveness of PEA for a variety of conditions. In the area of Parkinson’s disease there have been positive experiences, but no large-scale publicized studies. Because the substance is a body’s own supplement that can be used in combination with other medicine, and because there have been so many other studies with positive results, we give a green-orange light. We doubt there will ever be enough funding to organize large-scale studies, as nobody will make money on it… It cannot be a patented substance, but a body’s own molecule. Considering the positive results of cannabis on Parkinson’s disease, PEA looks like a good choice for people that don’t want to get stoned, but want the positive effects on their bodies’ endocannabinoid system.
Additional literature on neuroinflammation
Zipp, F. and Aktas, O. (2006) The brain as a target of inflammation: common pathways link inflammatory and neurodegenerative diseases. Trends Neurosci. 29, 518–527
Aktas, O. et al. (2005) Neuronal damage in autoimmune neuroinflammation mediated by the death ligand TRAIL. Neuron 46, 421–432 Block, M.L. and Hong, J.S. (2005) Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism. Prog. Neurobiol. 76, 77–98
Allan, S.M. et al. (2005) Interleukin-1 and neuronal injury. Nat. Rev. Immunol. 5, 629–640 Babcock, A.A. et al. (2003) Chemokine expression by glial cells directs leukocytes to sites of axonal injury in the CNS. J. Neurosci. 23, 7922– 7930
Marchetti, B. and Abbracchio, M.P. (2005) To be or not to be (inflamed) – is that the question in anti-inflammatory drug therapy of neurodegenerative disorders? Trends Pharmacol. Sci. 26, 517–525
 Morera-Herreras T, Miguelez C, Aristieta A, Ruiz-Ortega JÁ, Ugedo L. | Endocannabinoid modulation of dopaminergic motor circuits. | Front Pharmacol. | 2012 Jun 12;3:110. doi: 10.3389/fphar.2012.00110. eCollection 2012.
 Esposito E, Impellizzeri D, Mazzon E, Paterniti I, Cuzzocrea S. | Neuroprotective activities of palmitoylethanolamide in an animal model of Parkinson’s disease. | PLoS One. |2012;7(8):e41880. doi: 10.1371/journal.pone.0041880. Epub 2012 Aug 17.