Parkinson’s (the Michael J. Fox disease) is a progressive disorder that involves gradual die-off of nerve cells that produce dopamine, with resulting deterioration of cognition and movement. Though we naturally lose dopamine-producing neurons with age, Parkinson’s accelerates the process and involves much more drastic deficiencies.
Readers diagnosed with fibromyalgia and chronic fatigue syndrome will note that dysfunctional dopamine production has also long been implicated in their illnesses as well – with the latest ME/CFS research suggesting it is at the root of underperforming nerve clusters in the brain.(1,2,3)
But now researchers at Tel Aviv University (TAU) report they’ve developed a peptide that can preserve dopamine and stop the neuron killing – actually stop it cold.
They’ve also found that the peptide can be injected effectively or even absorbed through the skin, and have developed an adhesive patch for sustained transdermal delivery.
The team at TAU began with a study of mutations in a gene known as DJ-1 that are associated with accelerated loss of dopaminergic neurons and onset of Parkinson’s symptoms at a young age. Normally, DJ-1 protects cells from toxic stresses,(4) and mutation-associated loss of that protection is associated with neuronal death.
In hopes that “the ability to modify the activity of DJ-1 could change the progress of the disease,” the team set out to develop a peptide that mimics DJ-1’s normal function so as to protect dopamine-producing neurons, explains principal investigator Nirit Lev, a movement disorders specialist at Tel Aviv University’s Sackler Faculty of Medicine.
As they have recounted in the Journal of Neural Transmission and other journals, Dr. Nev and colleagues Dani Offen & Eldad Melamed explain that, using a short peptide based on the healthy version of DJ-1 itself as a vehicle, they:
• “Attached the DJ-1 related peptide to another peptide that would allow it to enter the cells, and be carried to the brain.”
• Tested the treatment on mice utilizing well-established toxic and genetic models for Parkinson’s disease.
• Discovered that, from both a behavioral and biochemical standpoint, the mice that received the peptide treatment showed remarkable improvement. Specifically:
– Symptoms such as mobility dysfunctions were reduced significantly,
– While dopamine-producing neurons were preserved and dopamine levels were increased in the brain.
Though many peptides have a short life span and degrade quickly, the researchers note that this peptide does not. Additionally, it provides a safe treatment option because peptides are organic to the body itself.
Overall, based on preclinical trials and hopefully human trials soon, their peptide treatment:
1. Mimics DJ-1’s normal function of protecting neurons
2. Stops neurodegeneration and supports higher dopamine levels in the brain.
3. Reduces problems with mobility in preclinical trials.
4. Could be developed as a preventive strategy that “can mean the difference between living life as a Parkinson’s patient or aging normally.”
5. May hold special promise for those with a genetic link to the disease who might opt for early testing, now that with the help of brain scans Parkinson’s may sometimes be diagnosed before motor symptoms begin.
Source: Based on American Friends Tel Aviv University news release, May 2, 2012
3. “An Elephant Among Us: The Role of Dopamine in the Pathophysiology of Fibromyalgia,” by Patrick B Wood, MD, and Andrew J Holman, MD. Journal of Rheumatology 36(2). Full text article, links to 33 other studies providing findings relevant to their theory.