Nu Skin teams with Dr. Cox to find a cure for Alzheimer's Part III - by Moxie Beauty Care

Dr. Cox is set to find a cure for Alzheimer's Part III

Moxie Beauty Care Admin

Doctor Paul Cox, creator of our epoch® beauty line, has set his goals pretty high. His research is very interesting and thought of sharing it with you. This article was published in the FORTUNE Magazine, enjoy the read of part III, and final, of a series!

Cox’s own work has now been cited by other researchers more than 12,000 times in scientific journals. But it’s the consortium as a whole that has really turned his initial insight about the Chamorro into an expansive body of research:

• In Sweden, neuropharmacologist Eva Brittebo ­revealed that rodents dosed with high levels of BMAA develop neurofibrillary tangles and behavioral aberrations—but only once they become adults, mimicking the long latency period seen in humans who develop Alzheimer’s.

• Dartmouth neurologist Elijah Stommel pinpointed epidemiological clusters of ALS around certain lakes in New England that have had cyanobacteria blooms.

• ALS expert Walter Bradley traveled with Cox to Qatar, where they found swaths of blue-green cyanobacteria laden with BMAA under the desert crust. They believe this might help explain a reported spike in ALS among U.S. veterans of 1991’s Operation Desert Storm. They have since found cyanobacteria under desert crust in Arizona and Utah.

• Algae biologist Larry Brand discovered that certain blue crabs off the coast of Florida that are commonly eaten by humans had levels of BMAA as high as the bats in Guam. “If BMAA were a man-made chemical,” Brand told me, “I don’t think it would ever be allowed to be added to food.”

• Cleveland Clinic neurologist Erik Pioro has plotted 1,000 cases of ALS in the northwest corner of Ohio, near Lake Erie, which is polluted with BMAA and several other neurotoxins.

All this research has inspired other scientists as well. A Norwegian team, for example, has looked at how BMAA affects proteins in zebra fish. In Canada, researchers have shown that BMAA is released from algae blooms as the cyanobacteria die. And in 2016, Chinese scientists showed that rats injected with BMAA developed ALS-like symptoms.

Despite such findings, the consortium’s work is far from accepted science. A 2017 review of the literature on BMAA by scientists at an EPA lab in North Carolina’s Research Triangle Park concluded that “the hypothesis of a causal BMAA neurodegenerative disease relationship is not supported by existing data.”

Undeterred, Cox has steered the focus of the Jackson lab to L-serine, which he believes could significantly delay the onset of Alzheimer’s and the progress of its symptoms. The FDA has previously approved the use of L-serine as a safe dietary supplement, and doctors sometimes prescribe it for chronic fatigue syndrome. The Cox team believes ­L-serine may play a neuroprotective role.

When I met with Cox recently in New York City, he was quick to share some newly published lab research on the role L-serine plays at the cellular level. We spoke over breakfast at the dreary Times Square hotel he frequents when courting funders or accompanying his wife, Barbara, to Broadway shows. “Here’s what we now think is astonishing about ­L-serine,” Cox said. “It appears to be neuroprotective against all possible protein misfolding. It basically turns on a system in our brains that looks for unfolded proteins and is quickly poised to act on them.”

Dr. Cox Study to cure Alzheimer's - Nu Skin by Moxie

For Cox, the most powerful illustration of L-serine’s potential is a 2016 study he and the University of Miami’s Mash oversaw on St. Kitts in the British Virgin Islands. A team at an animal research lab there fed bananas loaded with BMAA, L-serine, or a combination of both to vervet monkeys who have a gene that is thought to increase the risk of Alzheimer’s in humans. (The control group got bananas with rice flour.) Monkeys given BMAA showed both the plaques and tangles common to Alzheimer’s patients. But those given an accompanying dose of L-serine had 80% to 90% fewer tangles in their brain tissue, the study found. The results astounded Mash and Cox, so they repeated the effort with another 140 vervets and got comparable results. Their findings were published in the Proceedings of the Royal Society.

Early in 2017, Cox published the results of a six-month clinical trial of L-serine given at varying doses to ALS patients. The Phase I trial, conducted by independent labs in San Francisco and Phoenix, showed once again that L-serine is safe for humans. One piece of data dangled alluringly from the paper, which was published in a respected ALS journal. The four patients who received the highest doses of L-serine (30 grams per day) saw the progress of their symptoms, as measured on a widely used scale known as ALSFRS-R, slow by 85%. The number of patients, in this case, was too small for the finding to reach statistical significance, but if further clinical trials replicate anything close to that percentage, L-serine would slow the progress of symptoms far more than any existing drug, potentially buying patients years of life. (The average ALS patient dies 2½ years after diagnosis.)