Treat Alzheimer’s Disease With Arginine
The study—published in the Journal of Neuroscience—is attracting national attention for proposing a new potential cause of Alzheimer’s disease. Duke researchers, who discovered a way to make the brains of mice respond to Alzheimer’s disease similarly to humans, found that in mice with the disease, immune system cells meant to protect the brain start to consume an important nutrient: arginine. They were able to slow disease progression in the mouse model with a small-molecule drug—indicating the eventual potential for a new treatment strategy.
Past research of the disease has focused on a protein called beta-amyloid, which creates plaques in the brain, rather than arginine.
“With drugs that affect amyloid, not a single trial has succeeded,” said Carol Colton, an author of the study and professor of neurology at the School of Medicine. “It’s time we look at new direction—and this is a potential direction that nobody has thought of before.”
Although Colton has been researching the immune system’s role in Alzheimer’s for many years, the breakthrough came when she was able to develop a mouse model that was more representative of the disease in humans than other models in the field.
Previously, genetic mutations given to mice led to the development of plaques in the brain, but failed to replicate the most important aspects of Alzheimer’s, including neuron death and memory loss, Colton explained.
“That’s always been frustrating for the field—you couldn’t really use mice as a springboard for treatment, because you have nothing to block,” said Matthew Kan, a seventh-year MD/PhD student. “It’s difficult to study the brain in a living person, but by changing this one gene to make the mice’s immune systems look more like humans’, we can now ask these questions in mice that we could in humans.”
In the more human-like system, researchers were able to observe the mice as they grew old and developed Alzheimer’s disease. They noted that the immune systems of mice with Alzheimer’s disease were suppressed, and found low levels of arginine in their brains.
The team then developed and tested a new drug in the mice, which blocked the immune pathway that consumes arginine in the brain. The treated mice showed significantly less memory loss and brain cell death than the untreated ones after 24 weeks, Colton noted. Although the team has developed a successful preventative therapy for mice, they are wary of jumping to conclusions.
“I, as a clinician, cringe at some of the reporting that I know is going to lead to a lot of false hope,” said James Burke, associate director of the Bryan Alzheimer’s Disease Research Center at Duke. “If you have a family member with the disease, you get the idea that this is the next cure.”
Burke emphasized that early animal studies are difficult to predict because a number of things could go wrong before treatment even reaches humans. But the study’s potential implications for Alzheimer’s therapy are still important for opening up the field to novel mechanisms, he said.
Moving forward, the researchers hope to continue testing the drug’s effectiveness in treating and reversing the Alzheimer’s condition in mice, although testing the treatment in human clinical trials might be anywhere from seven to more than 10 years away, Colton said.
”I think there’s still a lot of work for us—to show what we’ve found in the mice is really what’s happening in humans,” Kan said. “But we have a great new direction to go in, and a lot of questions to ask.”
According to Lane Simonian, arginine could be a symptom and a byproduct of Alzheimer’s disease. Lane posted the following response to the article above:
High levels of arginase activity are a symptom rather than a cause of Alzheimer’s disease. It is a product of high levels of peroxynitrites and hydrogen peroxide which are the likely causes of the disease. Arginase activity may be a protective effort by the brain because it limits the amount of inducible nitric oxide produced in the brain via arginine (inducible nitric oxide combines with superoxides to produce peroxynitrites). Similarly amyloid plaques are a protective effort by the brain because they absorb the copper and zinc that stimulate the enzyme (superoxide dismutase) that converts superoxides to hydrogen peroxide.
Peroxynitrites inhibit the synthesis and release of neurotransmitters involved in short-term memory, sleep, mood, social recognition, and alertness, inhibit blood flow and the transport of glucose in the brain which can result in apathy, wandering, and delusions, overactivate and then sometimes deactivate NMDA receptors resulting in hallucinations, prevent the regeneration of neurons in the hippocampus, and via DNA damage and energy deprivation leads to the death of neurons.
Most of the above damage can be at least be partially reversed with strong peroxynitrite scavengers. Some of these scavengers such as eugenol in rosemary essential oil via aromatherapy and ferulic acid, syringic acid, vanillic acid, p-coumaric acid, and maltol have led to improvements in cognitive function in Alzheimer’s patients.
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Gary Chandler is a prion expert. He is the CEO of Crossbow Communications, author of several books and producer of documentaries about health and environmental issues around the world. Chandler is connecting the dots to the global surge in neurodegenerative disease, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and other forms of prion disease. The scientific name for prion disease is transmissible spongiform encephalopathy.