Alzheimer's disease, Cancer, Featured, Longevity, Neurocognitive disorders, Neuroscience

New treatment stops progression of Alzheimer’s disease in monkey brains

According to a new study, a novel medication causes immune defense cells to swallow malformed proteins, amyloid beta plaques, and tau tangles, which are known to damage surrounding brain cells in Alzheimer’s disease.

The study, led by NYU Grossman School of Medicine experts, found that after treatment with CpG oligodeoxynucleotides (CpG ODN), old monkeys had up to 59 percent less plaque deposition in their brains than untreated animals. Protein pieces form amyloid beta plaques, which clump together and obstruct nerve cell connections (neurons).

The levels of toxic tau in the brains of treated rats also decreased. When disease-related alterations to the chemical structure of this nerve fiber protein allow it to bind to other cells, it can kill nearby tissue.

“Our findings illustrate that this therapy is an effective way of manipulating the immune system to slow neurodegeneration,” says Akash Patel, MS, an assistant research scientist in the Center for Cognitive Neurology at NYU Langone Health.

According to the researchers, the therapy had cognitive benefits as well. When given a series of problems, old monkeys who had been given the medicine performed similarly to young adult animals and far better than those in their age group who had not been given the medicine. The monkeys that were given the treatment learnt new puzzle-solving skills faster than their contemporaries who were not.

Previous treatments aimed at the immune system have failed, according to experts, because the medications overstimulated the system, generating hazardous levels of inflammation that can damage brain cells.

“Our new treatment avoids the pitfalls of earlier attempts because it is delivered in cycles, giving the immune system a chance to rest between doses,” says study co-senior author Thomas Wisniewski, MD. In the treated monkeys, he observes no extra inflammation. Wisniewski is the Gerald J. and Dorothy R. Friedman Professor of Neurology at NYU Langone, as well as the head of the Center for Cognitive Neurology.

Alzheimer’s disease is the sixth most common cause of death in the United States, and there is currently no treatment. Drug therapy aimed at slowing or managing the symptoms have failed, according to Wisniewski, who is also the head of NYU Langone’s Alzheimer’s Disease Research Center. The immune system, which is made up of cells and proteins that protect the body from germs and viruses, has been linked to Alzheimer’s disease by an increasing body of data. The innate immune system has a group of immune cells that consume and eliminate trash and poisons from body tissues, as well as invading pathogens. According to studies, as people age, their immune defenses grow sluggish and fail to eliminate poisons that trigger neurodegeneration.

According to Wisniewski, the new study, which was published as a cover story in the journal Brain on June 15, is the first to target the innate immune system as a possible cure for the condition in monkeys. The CpG ODN medicines belong to a family of innate immune regulators that help these tired immune guardians get back on their feet. According to him, the study team is also the first to employ the “pulsing” medicine administration strategy to avoid excessive inflammation, which is caused by immune cells homing in on sites of damage or infection, resulting in swelling and discomfort. While inflammation is required for immunological defenses and healing, it also contributes to numerous disease pathways.

The research team looked at 15 female squirrel monkeys aged 17 to 19 years old for the study. The medicine was given to eight people once a month for two years, while the other were given a saline solution. The researchers watched the two groups’ behavior and compared plaque deposition, tau protein levels, and inflammatory evidence in brain tissue and blood samples.

Almost all squirrel monkeys acquire a kind of neurodegeneration that mimics Alzheimer’s disease in people as they age, according to Wisniewski, making them ideal for researching the condition.

“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-senior author Henrieta Scholtzova, MD, Ph.D.

Scholtzova, an associate professor in NYU Langone’s Department of Neurology, points out that the researchers only looked at aged monkeys that already exhibited evidence of neurodegeneration. She points out that more research on younger animals would allow them to examine the treatment’s efficacy at an earlier stage of the illness.

According to Scholtzova, the team wants to try CpG ODN treatment on human patients with minor cognitive deficits or dementia in the early phases. They also plan to investigate this therapy in the context of other neurodegenerative diseases.

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