2024-08-16 06:00:03
A new compound could revolutionize the treatment of Alzheimer’s disease.
Researchers at the University of California, Los Angeles (UCLA) have developed a molecule that can restore cognitive function and memory in mouse models of the disease. This breakthrough marks a departure from traditional approaches that focus on removing amyloid plaques from the brainoften considered responsible for the symptoms of the disease.
Alzheimer’s treatments have long aimed to reduce the buildup of beta-amyloid protein plaques in the brain, according to the “amyloid cascade” theory. Although these treatments slow the progression of the disease, they fail to reverse cognitive impairment that is already present. Istvan Mody, professor of neurology and physiology at UCLA, points out that these treatments leave the brain “perhaps plaque-free,” but with neural circuits still altered. In response, Istvan Mody and his team have developed a new compound, called DDL-920, that targets a different biomolecular mechanism. Their approach relies on stimulating gamma oscillations, high-frequency electrical signals that are essential for memory and cognitive functions. These oscillations are generated by fast interneurons, parvalbumin neurons, which play an essential role inactivation neural circuits involved in cognitive processes. However, in Alzheimer’s patients, these oscillations are often diminished, even before amyloid plaques begin to alter the brain.
Previous studies had attempted to restore these gamma oscillations using sound or visual stimulation, but the results were inconclusive in terms of cognitive improvement. So Istvan Mody and his colleagues explored a pharmacological route. By inhibiting the receptors that reduce gamma oscillations, DDL-920 would allow neurons to function more efficiently, thereby restarting the oscillations necessary for memory.
To test the effectiveness of this molecule, the researchers administered DDL-920 to mice genetically modified to reproduce the symptoms of Alzheimer’s disease. After two weeks of treatment, the treated mice showed cognitive performance comparable to that of healthy mice in a maze test. In addition, no behavioral abnormalities were observed.
While these results are promising, further research is needed to confirm the safety and efficacy of this treatment in humans. If this research proves successful, this compound could pave the way for new therapies for other diseases associated with reduced gamma oscillations, such as depression and schizophrenia.
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