Minocycline, a tetracycline derivative, prevented degeneration in dopamine-producing brain cells in mice that were made to have a Parkinson's-like disease. Parkinson's is marked by the destruction of brain cells that produce dopamine, a chemical that is a key regulator of muscle movement.
The brain damage his team induced in the study mice certainly doesn't mimic the exact cause or course of Parkinson's disease.
Moreover, the animals required very high doses of oral minocycline for it to protect the brain -- doses that may not be "achievable" in patients. If this research can be extended to humans, a better approach would likely be to develop a different tetracycline that "gets into the brain better.
Parkinson's disease is a motor system disorder in which patients experience tremors, muscle rigidity, impaired movement, and problems with balance and coordination. Treatment includes drugs that replace the brain's dwindling supply of dopamine, but there is no cure for the progressive loss of dopamine-producing brain cells.
The researchers treated mice with MPTP, a toxic chemical that induces parkinsonian symptoms in animals and humans. Groups of mice were treated with minocycline before, during and after receiving MPTP. Some mice did not receive the antibiotic.
The investigators found that at high doses, the drug was able to protect many dopamine cells from damage when it was given either before or after MPTP.
Similarly, the researchers note, a recent study showed that minocycline delayed death in mice made to show characteristics of Huntington's disease, a genetic disorder that is also marked by brain cell degeneration.
Minocycline may prevent dopamine-cell damage by blocking the action of nitric oxide (NO) in the brain. Some research has suggested that the release of NO from activated brain cells called glial cells is involved in the degeneration seen in Parkinson's. This remains only speculation, however.
Whatever the reason, minocycline seems to have "neuroprotective effects quite apart from its antibiotic properties.
Proceedings of the National Academy of Sciences December 4, 2001;98:14669-14674
Quite an interesting development. I have been using Minocin for over a dozen years to successfully treat thousands of patients with rheumatoid arthritis.
Many "experts" doubt that the Minocin is working as an antibiotic but speculate that in rheumatoid arthritis the drug has some anti-collagenase activity to explain its beneficial actions.
This may be true, but directly opposes Dr. Brown's many decades of experience in which he successfully treated over 10,000 patients with antibiotics.
If you read my protocol below you will find that I have significantly modified the antibiotic protocol to include application of the eating plan and now NST and most recently EFT.
It is my speculation that there is indeed an infection going on, usually a mycoplasma, that seems to be most typically present as a result of accumulated unresolved stresses and emotional traumas that have compromised the immune system, making it susceptible to this infection.
The study above is the first suggestion I am aware of that Minocin might also be useful in Parkinson's and I will likely start using it for those patients.
Although the authors doubt an infectious component, and they may be right, my common sense suggests that they may be incorrect and that we may be dealing with an atypical cerebral mycoplasma infection.
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