New Alzheimer's Treatment Shown To Stop Disease's Progression In Monkey Brains

Elderly squirrel monkeys with neural degeneration received the new treatment and experienced improved cognitive function and fewer dangerous plaque build-ups than their untreated friends. Image credit: Ludmila Ruzickova/Shutterstock.com

A new therapy has been shown to stop the progression of Alzheimer’s disease in monkeys, according to a new study published in the journal Brain.

Alzheimer’s disease is a progressive condition that affects the brain. Proteins build up between nerve cells, forming abnormal structures called plaques and tangles. This leads to the death of nearby brain tissue, resulting in the progressive loss of cognition involving memory problems, speech and spatial confusion, and mood dysfunction. It is the most common cause of dementia in older adults, and the sixth-highest cause of death in the United States – third-highest among older adults.

Although Alzheimer’s has no known cure, research in recent years has pointed to the immune system as contributing to its development. Studies have shown that there are certain types of immune cells found within the innate immune system – the immune system we are born with, rather than picking up through exposure to disease or vaccines – which are responsible for clearing away toxins from the body. But as we age, these cells get lazy. They stop clearing away all the toxins from bodily tissues, leading to a build-up that can cause neurological degeneration.

That’s why this new therapy, pioneered by researchers at the NYU Grossman School of Medicine, targets the immune system directly. The scientists made use of a drug with the snappy name of CpG oligodeoxynucleotides (CpG ODN), which prompts the immune system to swallow the amyloid beta plaques and tau tangles that are responsible for brain cell death.

“Our findings illustrate that this therapy is an effective way of manipulating the immune system to slow neurodegeneration,” study co-author Akash Patel said in a statement. Subjects that received treatment with immune regulating drugs were found to have up to 59 percent fewer plaque deposits in their brains than those who had not received the drug.

The scientists studied 15 female squirrel monkeys aged between 17 and 19 years old – very old by squirrel monkey standards. As they age, squirrel monkeys develop their own form of neurodegeneration which is similar to Alzheimer’s in humans, making them ideal for the experiment. The researchers gave eight of the monkeys a single dose of the CpG ODN drug once a month for two years – the other seven received a saline solution (even monkey studies need to guard against the placebo effect.)

The results were clear: not only did the monkeys that received the treatment have fewer plaque build-ups, but they also performed much better in cognitive exercises than their unmedicated chums. They were also able to learn new puzzle-solving skills – a talent Alzheimer’s disease can severely impair – faster than the untreated cohort.

The therapy is innovative not because of the drug itself, but because of the delivery. Previous research has attempted to target the immune system, the researchers explained, but failed when the high doses of medication involved overstimulated the immune system. This led to inflammation, which itself kills brain cells.

“Our new treatment avoids the pitfalls of earlier attempts because it is delivered in cycles,” explained study co-senior author Thomas M. Wisniewski. “[This gives] the immune system a chance to rest between doses.”

So far, explained study co-senior author Henrieta Scholtzova, the team’s results are limited to elderly monkeys with advanced neurodegeneration, so the next priority is to trial the therapy in younger animals with milder symptoms. The researchers also hope to start trialling the new therapy in humans who are in the first stages of dementia.

“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,” Scholtzova said.


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