A new therapy with CpG oligodeoxynucleotides (CpG ODN) has been shown to stimulate immune defense cells to engulf deformed proteins, beta amyloid plaques is tangles by tau, the accumulation of which is known to suppress brain cells.
The new Research was published in the scientific journal Brain.
CpG ODN drug: this is how it works
The experiment was developed by the scientists of the NYU Grossman School of Medicine, and highlighted that elderly monkeys had up to 59% less plaque deposits in the brain after treatment with CpG oligodeoxynucleotides (CpG ODN), compared to untreated animals. Beta amyloid plaques are protein fragments that aggregate and obstruct the junctions between nerve cells (neurons).
The brains of the treated animals also experienced a drop in toxic tau levels: “Our results illustrate that this therapy is an effective way of manipulating the immune system to slow neurodegeneration.“, has explained Akash Patel, MS, research assistant at the Center for Cognitive Neurology at NYU Langone Health.
The heads of the study also specified that the treatment also resulted in cognitive benefits. When a series of puzzles were presented, the older monkeys given the drug performed similarly to the young adult animals and far better than those of their age group who were left untreated. The treated monkeys also learned new puzzle-solving skills faster than their untreated peers.
“Our new treatment avoids the pitfalls of previous attempts because it is administered in cycles, giving the immune system a chance to rest between doses.Says the study’s senior co-author Thomas Wisniewski, professor at the Department of Neurology and director of the Center for Cognitive Neurology at NYU Langone.
Alzheimer’s disease does not yet have a known cure. Drug therapies developed to slow or manage symptoms have failed, explains Wisniewski, who is also director of theAlzheimer’s Disease Research Center of NYU Langone. A growing body of evidence has implicated that the immune system, the set of cells and proteins that defend the body from invasion by bacteria and viruses, contributes to Alzheimer’s. A subset of immune cells, those within the innate immune system, remove debris and toxins from body tissues along with invading microbes. Previous research has highlighted how these immune keepers become sluggish as a person gets older and are unable to eliminate the toxins that cause neurodegeneration.
This new research, however, is the first to concern itself with the innate immune system: CpG ODN drugs are part of a class of innate immune regulators that accelerate these worn-out immune guardians. the research team explained that it is also the first to use the drug administration technique “button”To avoid excessive inflammation, immune responses such as swelling and pain that result from the homing of immune cells to the sites of injury or infection. Although necessary for immune defenses and healing, too much inflammation contributes to many disease mechanisms.
The scientific experiment involved 15 female squirrel monkeys between the ages of 17 and 19. Eight received a single dose of the drug once a month for two years, while the others were given saline solution instead. The researchers observed the behavior of the two groups and compared brain tissue and blood samples for plaque deposits, tau protein levels, and evidence of inflammation.
“The similarities in aging between the animals studied and our own species give us hope that this therapy will also work in human patients.Says the study’s senior co-author Henrieta Scholtzova, MD, Ph.D. The scientist specified that the researchers only evaluated older monkeys that already showed significant signs of neurodegeneration. Further testing on younger animals, he notes, would allow them to assess the effectiveness of treatment in earlier stages of the disease.
This study will go on and Scholtzova states that the team plans to begin testing ODN CpG therapy on human patients with mild cognitive impairment or in the early stages of dementia. They also intend to study this treatment in related neurodegenerative diseases.