In a groundbreaking study published in The Proceedings of the National Academy of Sciences, researchers at UCLA Health have identified and synthesized a molecule that could restore cognitive functions in mice with Alzheimer’s-like symptoms.
This molecule, named DDL-920, has shown the ability to effectively restart the brain’s memory circuits, a finding that could lead to a novel treatment approach for Alzheimer’s disease.
Alzheimer’s disease is a devastating condition that leads to memory loss and cognitive decline. Current treatments, such as lecanemab and aducanumab, focus on removing harmful plaques that build up in the brains of Alzheimer’s patients.
While these treatments slow the progression of cognitive decline, they do not restore lost memory or cognitive function. DDL-920, however, works differently.
According to Dr. Istvan Mody, the study’s lead author and a professor of neurology and physiology at UCLA Health, “There is really nothing like this on the market or experimentally that has been shown to do this.”
Unlike existing drugs that target plaque, DDL-920 directly addresses the brain’s memory circuits. These circuits are essential for cognitive functions, and in Alzheimer’s patients, they often become disrupted.
The brain uses different rhythms, similar to a traffic signal, to control various functions. Gamma oscillations, which are among the fastest brain rhythms, play a key role in memory and cognitive processes. In patients with early Alzheimer’s symptoms, these gamma oscillations are reduced, leading to memory problems.
Previous attempts to restore memory through external stimulation, such as using light, sound, or magnetic pulses, have had limited success. While these methods helped dissolve brain plaques, they did not significantly improve cognitive function.
Mody and his team decided to take a different approach. Instead of using external tools to stimulate the brain, they looked for a way to trigger these rhythms from within the brain itself.
Their research focused on a specific type of neuron, called parvalbumin interneurons, which are crucial for generating gamma oscillations. These neurons are regulated by receptors that respond to GABA, a chemical messenger in the brain.
However, these receptors can act like brakes, reducing the neurons’ ability to produce strong gamma oscillations. The team identified DDL-920 as a compound that can block these receptors, allowing the neurons to maintain powerful gamma oscillations.
To test whether DDL-920 could improve memory and cognitive function, the researchers used genetically modified mice that exhibit Alzheimer’s-like symptoms.
These mice, along with normal mice, were tested in a Barnes maze, a circular platform with visual cues and one escape hole. This maze is commonly used to measure how well rodents can learn and remember the location of the escape hole.
After the initial tests, the Alzheimer’s model mice were given DDL-920 twice daily for two weeks. Remarkably, after the treatment, these mice were able to remember the location of the escape hole just as well as the normal mice.
Furthermore, the treated mice did not show any abnormal behavior or side effects during the two-week treatment period.
Dr. Mody emphasized that while these results are promising, much more research is needed to determine if DDL-920 would be safe and effective in humans.
If it proves successful, this treatment could also be explored for other conditions associated with reduced gamma oscillations, such as depression, schizophrenia, and autism spectrum disorder.
“We are very enthusiastic about that because of the novelty and the mechanism of action that has not been tackled in the past,” Mody said.
This discovery represents a significant step forward in the search for treatments that not only slow down Alzheimer’s disease but also restore lost memory and cognitive function.
If you care about Alzheimer’s disease, please read studies about the protective power of dietary antioxidants against Alzheimer’s, and eating habits linked to higher Alzheimer’s risk.
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The research findings can be found in Science Translational Medicine.
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