New Hope for Alzheimer's: Sleep Drug Slows Disease Progression
Researchers have discovered a promising approach to potentially slow or even prevent Alzheimer's disease progression. The key lies in targeting sleep disturbances, which are now understood to play a significant role in the disease's advancement.
Alzheimer's disease is marked by two primary hallmarks: amyloid plaques and tau protein tangles. While amyloid plaques have long been the focus, recent findings suggest that tau pathology correlates more closely with brain atrophy and cognitive decline. These twisted tangles disrupt nutrient and information flow within brain cells, leading to their deterioration.
In a breakthrough, the insomnia medication Lemborexant has shown potential in reducing brain damage associated with Alzheimer's. This drug works by targeting the orexin system, which regulates wakefulness, appetite, and arousal. In neurodegenerative conditions like Alzheimer's, this system becomes dysregulated and overactive, leading to chronic sleep fragmentation and excessive daytime sleepiness. This, in turn, accelerates the accumulation of toxic proteins in the brain.
In laboratory models, Lemborexant reduced tau buildup and restored healthier sleep patterns. The medication preserved brain structure and prevented shrinkage typically seen in Alzheimer's disease progression. It does this by preventing the accumulation of toxic tau proteins that destroy neurons and cause cognitive decline. Notably, Lemborexant works through the orexin signaling pathway, which is linked to neurodegenerative diseases.
While Lemborexant is currently available for sleep disorders, its potential in treating Alzheimer's disease is promising. Further research and clinical trials are needed to confirm these findings and explore the drug's potential as a disease-modifying therapy. It's important to note that no public information suggests Eisai, the company developing Lemborexant, is focusing on Alzheimer's disease specifically or has achieved outstanding success in reducing brain damage caused by tau proteins.
