A new treatment stops the progression of Alzheimer’s disease in monkey brains


Outline of the brain of a person with Alzheimer’s disease. Credit: Wikipedia / public domain.

A new therapy causes immune defense cells to swallow deformed proteins, amyloid beta plaques and tau messes, which are known to accumulate nearby brain cells as part of Alzheimer’s disease, according to a new study.

Led by researchers at the NYU Grossman School of Medicine, the research showed that older monkeys had up to 59 percent fewer plaque deposits in the brain after treatment with CpG oligodeoxynucleotides (CpG ODN) compared to untreated animals. . These they are fragments of proteins that bind and clog joints (neurons).

The brains of the treated animals also had a decrease in toxic tau levels. This nerve fiber protein can destroy neighboring tissues when disease-related changes in its chemical structure cause it to trap other cells.

“Our findings illustrate that this therapy is an effective way to manipulate the to curb neurodegeneration, ”says Akash Patel, EM, an assistant researcher at NYU Langone Health’s Center for Cognitive Neurology.

Researchers say the treatment also brought cognitive benefits. When presented with a series of puzzles, the elderly monkeys who had the drug performed similarly to young adult animals and much better than those in their age group who had not been treated. Treated monkeys also learned new puzzle-solving skills faster than their untreated peers.

According to the researchers, previous treatment efforts targeting the immune system failed because the drugs overstimulated the system, causing dangerous levels of inflammation that can kill brain cells.

“Our new treatment avoids the pitfalls of previous attempts, as it is delivered in cycles, giving the immune system a chance to rest between doses,” says Thomas Wisniewski, MD, co-author of the study. He points out that no additional inflammation has been seen in the treated monkeys. Wisniewski is Professor Gerald J. and Dorothy R. Friedman of the Department of Neurology and director of the Center for Cognitive Neurology at NYU Langone.

Alzheimer’s disease is the sixth leading cause of death in the United States and has no known cure. Pharmacological therapies designed to slow or control symptoms have failed, says Wisniewski, also director of the Center for Alzheimer’s Disease Research at Langone University in New York. A growing body of evidence has implicated the immune system, the set of cells and proteins that defend the body from the invasion of bacteria and viruses, as a contributor to Alzheimer’s disease. A subset of immune cells, those of the innate immune system, swallow and remove waste and toxins from body tissues along with invasive microbes. Studies have shown that these immune custodians become slow as a person ages and does not eliminate the toxins that cause neurodegeneration.

The new research, published as a cover article on June 15 in the journal Brain, is the first to target the innate immune system with potential therapy for the monkey disorder, according to Wisniewski. CpG ODN drugs are part of a class of innate immune regulators that streamline these worn out immune guards. According to him, the research team is also the first to use the technique of administering drugs “pulsing” to prevent excessive inflammation, immune-driven responses, such as inflammation and pain, which result of the insertion of immune cells at the sites of injury or infection. Although necessary for immune defenses and healing, excessive inflammation contributes to many mechanisms of the disease.

For the research, the research team studied 15 female squirrel monkeys aged 17 to 19 years. Eight received a single dose of the drug once a month for two years, while the rest were given saline. The researchers observed the behavior of the two groups and compared brain tissue and blood samples for plaque deposits, tau protein levels, and inflammation tests.

Wisniewski notes that as they age, virtually all squirrel monkeys naturally develop a form of neurodegeneration that mimics Alzheimer’s disease in humans, making them ideal for studying the disease.

“The similarities in aging between the animals studied and our own species give us hope that this therapy will work in human patients as well,” says study co-author Henrieta Scholtzova, MD, Ph.D.

Scholtzova, an associate professor in the Department of Neurology at NYU Langone, warns that the researchers only evaluated elderly monkeys that already showed significant signs of neurodegeneration. According to her, further testing in younger animals would make it possible to evaluate the effectiveness of treatment in earlier stages of the disease.

Scholtzova says the next team plans to start testing ODC CpG therapy in human patients with mild cognitive impairment or in early stages of dementia. They also intend to study this treatment in related neurodegenerative diseases.

Targeted immune boosting eliminates toxic proteins from Alzheimer’s disease mouse model

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Citation: A new treatment stops the progression of Alzheimer’s disease in monkey brains (2021, June 15) recovered on June 15, 2021 at https://medicalxpress.com/news/2021-06-treatment-alzheimer- disease-monkey-brains.html

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