Researchers have discovered that the aggregation of amyloid-β, a protein widely believed to initiate Alzheimer’s disease, disrupts the circadian rhythm in supporting cells of the brain, offering new insight into the complex pathology of the disease.

Circadian rhythm, the body’s internal clock that regulates daily cycles of gene expression and cellular activity, is essential for proper tissue function. Previous studies have shown that this rhythm becomes disrupted with age and in age-related diseases. However, the mechanisms behind these disruptions have remained unclear.

The new study reveals that misfolded amyloid-β proteins interfere specifically with the circadian rhythm in non-neuronal supporting cells in the brain. This disruption adds a critical layer to understanding how Alzheimer’s disease affects the brain beyond the well-known neuronal damage, highlighting the importance of synchronized rhythms among different cell types and tissues.

These findings suggest that Alzheimer’s disease pathology extends beyond neurons to the supporting cells that help maintain healthy brain function. Understanding how amyloid-β affects circadian regulation may open new avenues for therapies that target these broader cellular disruptions.”

The study underscores the growing recognition that circadian rhythm plays a pivotal role in brain health and disease and offers a fresh perspective on the complex processes contributing to Alzheimer’s disease.