Sleep Deprivation Damages Myelin, University of Camerino Study Finds

Sleep deprivation and myelin integrity

A study headed by researchers at the University of Camerino in Italy has found that going without sleep can damage the fatty insulation that protects neurons, undermining mental processing.

Using a range of experiments and assessments, the team traced this damage to chemical disturbances in oligodendrocyte cells. These cells manage the cholesterol that makes up an important component of myelin, the protective coating around nerve fibres.

"This study identifies oligodendrocytes as key mediators by linking sleep deprivation to impaired myelin integrity, slowed nerve conduction, and behavioral deficits," write the researchers in their published paper.

MRI evidence and sleep quality

The scientists examined MRI scans from 185 healthy volunteers. Their analysis supported earlier research showing that the integrity of the brain's white-matter structures declined as participants self-reported poorer sleep habits.

The researchers next tested rats that had been deprived of sleep for 10 days. Although the nerve fibres in the animals' brains did not change in size, the myelin sheath surrounding each neuron's trunk, known as an axon, was thinner than in a control group.

Additional experiments showed that signalling between particular brain regions was approximately one-third slower in the sleep-deprived rats. Lack of sleep also reduced synchronisation between regions of the brain.

Oligodendrocytes, cholesterol and slower neural communication

Axons are essential to neural communication. As demonstrated by memory and exercise tests in the rats, sleep loss thins myelin, slowing communication between neurons and increasing the likelihood of mental fatigue and fogginess.

A genetic analysis performed on the mice showed that oligodendrocytes were no longer processing cholesterol as efficiently as they normally would.

"Our findings highlight a possible role of oligodendrocyte cholesterol dysregulation in behavioral deficits associated with sleep loss and unveil a novel target for intervention," write the researchers.

The team went further by treating the sleep-deprived rats with cyclodextrin, a drug intended to restore cholesterol transfer. This produced improvements in both movement and memory, supporting their explanation of the process.

Most of this work, however, relied on animal models, meaning future studies will need to confirm the findings in humans. Despite this limitation, the results point to an intriguing mechanism through which insufficient sleep can leave us feeling sluggish.

In time, these findings could help guide treatments that reduce some effects of sleep loss in people for whom it is a chronic condition, which has also been associated with a variety of later health problems.

"The increasing prevalence of sleep deprivation poses a public health challenge in modern society," write the researchers.

"Manifestations of reduced alertness, such as slowed reaction times and increased errors, are well-documented behavioral indicators of sleep loss."

The research was published in PNAS.