New Delhi: Improving sleep by enhancing the body’s natural circadian rhythms can help the brain recover after a stroke, which may provide a new strategy for enhancing waste removal from the brain and its outcomes, according to a new study.
The results, published in the Journal of Clinical Investigation, show that the interventions aim to enhance the body’s natural state Circadian rhythmssuch as timely exposure to light, melatonin or a drug that targets the body clock, has led to improved recovery in mouse models of stroke.
Researchers from the University of Rochester Medical Center also found improvements in Glymphatic system – Waste disposal network in the brain – and lower levels Inflammatory molecules Which can remain in the brain after a stroke.
The system moves cerebrospinal fluid along blood vessels and through brain tissue, delivering nutrients and helping to remove waste and inflammatory signals.
“discussion Stroke recovery “It really starts with the idea that stroke is not just a vascular event, but also a timing disturbance,” said lead author Lauren Hablitz, a neuroscientist at the University of Rochester Medical Center.
Strokes are considered to follow predictable patterns during the time of day, with them being more likely to occur in the morning. It can also often be more serious towards the end of the sleep period.
Meanwhile, many stroke patients experience disrupted sleep-wake cycles after their injury, and these disturbances are associated with poor recovery, depression, and decreased quality of life, the researchers said.
“This led us to ask a simple question. If timing is broken after stroke, can we improve recovery by boosting the circadian clock?” Hablitz said.
The researchers added that previous studies show impaired function of the glymphatic system after a stroke, which may limit the brain’s ability to remove harmful molecules that accumulate during recovery.
The team evaluated interventions known to affect the body’s internal clock, including timed light exposure, melatonin, a clock-targeting drug called KL001, and time-restricted feeding — each of which can enhance glymphatic function in healthy animals.
The “promising” approaches – KL001 and time-restricted feeding – were then tested in mouse models of stroke.
The researchers said that treatment began three days after the stroke, which exceeds the narrow treatment period for clot-busting drugs and other acute interventions.
However, despite the delay, animals that received the intervention showed improved motor recovery, smaller lesion sizes, enhanced glymphatic flow, and lower levels of inflammatory cytokines in the brain.
“The cytokines all moved in the same direction,” Hablitz said. “This suggests that we may not be targeting a specific inflammatory pathway. Instead, we may be helping the brain remove inflammatory signals more effectively.”
The team said the findings could have practical implications for stroke rehabilitation, as a promising intervention includes time-restricted feeding – a behavioral approach that is already being studied for obesity, diabetes and cardiovascular disease, among others.
They added that the findings are currently limited to animal models and that more work is needed to understand how circadian rhythms, glymphatic function and inflammation interact after stroke.
Moreover, the study reflects a growing shift in neuroscience that views sleep, circadian rhythms, and fluid transport as fundamental drivers of brain health, the researchers said.
