However, the next form of transmission we need to consider is transmission through blood and tissue. …read more
- Early detection may help researchers understand more about how the disease progresses, where it starts and how it spreads.
- It would allow patients to identify their premotor symptoms for what they are, and seek quicker relief of those symptoms.
- If detected early enough, neuroprotective strategies (some already known to researchers) may be able to halt progression before the onset of “overt PD”.
- Early detection will be important for future therapies that stop or slow the progression of Parkinson’s disease; these are the so-called “disease modifying” therapies. The earlier the detection, the more neurons could be saved.
These last two benefits are where …read more
According to investors, the most promising drugs in the pipeline for treating Parkinson’s disease DON’T actually treat the disease. The drugs merely reduce some of the symptoms of this degenerative disease. The sole purpose of one of the drugs is to reduce the side effects of another drug that itself only helps symptoms!
As the numbers of sufferers continues to increase, treatment of symptoms is certainly lucrative. But this report should remind us of the desperate need for treatments that slow, stop, or reverse the disease itself. Parkinson’s is progressive and more and more Continue reading
Since I’ve started working on this project, many people have asked me if Parkinson’s disease is “genetic or environmental”. One of the most frequently cited studies on this question looked at twin brothers: identical twins versus fraternal twins. If one twin got Parkinson’s, would the other twin get it as well?
If Parkinson’s was genetic, we would expect both identical twin brothers to get Parkinson’s more often than both fraternal twin brothers. Why is this? Because identical twins share much more genetic information than fraternal twins, who share as much genetic information as regular brothers. More genetic information means more likelihood that both identical twins will share traits, including disease risk, that are caused or influenced by heritable factors.
So what did the study find? …read more
Since I’ve started working on this project to slow Parkinson’s, quite a number of people have asked me about a dietary supplement called Coenzyme Q10, commonly abbreviated CoQ10. It is a natural substance in your body that is critical to mitochondria, the power generators in your cells.
CoQ10 has gained interest from the alternative health community because it also functions as a potent antioxidant for both lipids and proteins, and can also regenerate other antioxidants. Also, oral supplementation of CoQ10 is effective at replenishing the body’s concentrations of CoQ10. And since many disease conditions deplete CoQ10, an obvious way to help fight those diseases is to supplement with CoQ10.
Indeed, many studies have generated evidence suggesting that CoQ10 is beneficial for a number of conditions. It also may correct a potentially dangerous side effect of statin use, which reduces serum levels of CoQ10 dramatically. The desire for supplementation has increased steadily over the past 10 years, and prices have dropped.
Regarding Parkinson’s disease, there was the feeling that CoQ10 could be helpful because oxidative stress is involved in Parkinson’s disease, either as a cause or an effect, depending on the Parkinson’s subtype. Parkinson’s also involves the inability to properly dispose of old or damaged mitochondria (mitophagy), so the desire to keep mitochondria healthy was reasonable.
Like other diseases, patients with Parkinson’s disease are also deficient in CoQ10. Additionally, CoQ10 appears to be effective at protecting dopaminergic neurons and other brain tissue from certain toxins and other insults (neuroprotection). I suspect that CoQ10 supplementation may be useful as part of a prevention strategy for those who are at greater risk of developing Parkinson’s. Supplementation also appears to be useful for certain patients that experience headaches and migraines.
However, increasing mitochondrial longevity through CoQ10 supplementation might have value for only certain subtypes of Parkinson’s patients . For those patients, one would at least want to pair CoQ10 with a mitophagy inducer. Our algorithms are busy examining the data, looking for existing supplements and compounds that should be effective as mitophagy inducers.
Indeed, a large clinical trial of CoQ10 in Parkinson’s patients was stopped in 2011 because it failed to show any particular benefit. This was disappointing because a number of animal models showed significant benefit of CoQ10. It is important to note that these were general Parkinson’s patients, not segmented based on subtype. I would be curious if certain subtypes would see more benefit, but I’m skeptical that CoQ10 supplementation alone would slow Parkinson’s neurodegeneration significantly.
The experiment on humans was certainly worth doing, however Parkinson’s is not a single issue that can be slowed with a single supplement. By the time somebody is diagnosed, there is an avalanche of multiple issues, caused by problems in multiple pathways, requiring multiple directions of attack. Multiple supplements are required to attack Parkinson’s from these directions. Adding to this complexity is that Parkinson’s is made up of multiple subtypes, each with a different origin. The mission of this project is to determine exactly what combination of supplements, and in what quantities, would benefit the most patients.