Results in one field of study can often be successfully transferred to another field of study. Such may be the case for using enzyme therapy to successfully treat CTE.
The particular enzyme is Serrapeptase, a proteolytic enzyme belonging to serine proteases. NIH has shown it's effectiveness for relieving Alzheimer's disease pathophysiology in rats:
I believe that Serrapeptase may modulate the excess tau protein in the CTE brain, as well as decreasing brain AchE activity, TGF-β, Fas and IL-6 levels while increasing BDNF and IGF-1 levels in the manner described by the above NIH research.
I am a retired research scientist, age 84, having made various scientific discoveries over the years, including the discovery of a fundamental new field of physics called Electromagnetic Radiography (EMR). Although my research work has been in the physical sciences, I also do research in the medical field to better understand and treat my own health, as well as share the benefits of this knowledge with others.
I first became interested in Serrapeptase, and more broadly, enzyme therapy, three years ago when I discovered that my carotid arteries were 40 percent blocked. Western medicine has no therapy other than a dangerous surgical procedure when blockage reaches 80 or 90 percent. Enzyme therapy has been successfully used in Oriental medicine for some time, and to some degree, in European medicine (Dr. Hans Neiper, et al).
After taking 120,000 SPU Serrapeptase daily for 6 months, I had a follow-up ultrasound that showed normal blood flow in my carotid arteries. Serrapeptase had removed the plaque that was blocking my carotid arteries. Specifically, it had dissolved the fibrin (protein) binding the plaque together. Unexpectedly, Serrapeptase also removed scar tissue, including a scar that I had on my leg from a bicycle accident when I was a young boy.
An elderly friend who is a retired minister was diagnosed with dementia that was affecting his speech. On the chance that his dementia might be caused by a circulatory deficiency (vascular dementia), I proposed that he, too, should try Serrapeptase therapy. After six months, he had a two-day battery of tests by four dementia specialists who found no evidence of any dementia.
It was only later that I came across the NIH research. Instead of vascular dementia, my friend may have had early onset Alzheimer's. If so, Serrapeptase may well have reversed it by dissolving the beta amylase, etc.
More recently, my wife (age 75) was developing dementia. After three months of 120,000 SPU daily of Serrapeptase, my wife's symptoms have virtually disappeared. We now suspect that she, too, had early onset Alzheimer's that Serrapeptase reversed.
Coincidentally, we are letting Western medicine run it's course. Ultrasound and MRA have shown that her dementia was not caused by circulatory deficiency. MRI showed
some brain shrinkage, consistent with age. EEG showed two slight abnormalities. She is scheduled to do a 24-hour EEG. Also, she will be doing a PET scan.
Because enzyme therapy is not part of conventional Western medicine, we have not shared our own private research in this area. Instead, I'm expecting the battery of tests to show that she no longer has dementia, consistent with my own empirical observations of her obvious improvement.
Serrapeptase is not a drug, and there are no side effects. Everything else aside, I look upon Serrapeptase as being a great "longevity pill" by virtue of it's ability to prevent
the buildup of arterial plaque and prevent blood clots -- the principal culprits in heart attack and stroke. It may also negates the need for cholesterol therapy (statins).
There are peripheral benefits, as well. Cancer cells develop a thick protein coating to prevent attack by the immune system. Serrapeptase destroys that coating, allowing the immune system to attack cancer cells. Serrapeptase is a mild analgesic and has some anti-inflammatory properties. Although Serrapeptase is not a blood thinner, it amplifies the effects of blood thinners, so as to lower the therapeutic dosages of warfarin, aspirin, etc.
Serrapeptase is slow acting. It may take upwards of three months before the results begin to become evident.
One caveat: it is vitally important that Serrapeptase be taken on an empty stomach, least stomach acid destroy the enzyme. The capsules have a vegetable-based enteric coating designed to resist stomach acid and allow the capsule to be passed to the small intestine where the alkaline environment dissolves the coating, allowing the enzyme to enter the bloodstream. I recommend waiting at least two hours, or longer, after a meal. For acid stomach, or slow digestion, waiting until the middle of the night or early morning is even better. No food should be taken for at least an hour after taking Serrapeptase.
Because Serrapeptase for CTE therapy is an entirely new and untested approach, it may, or may not, help alleviate CTE. If it does, great! If not, no harm done. It is safe, there is no downside, and it promotes good arterial health by preventing blood clots and the buildup of plaque.