Study reports that sleep modulation interventions that facilitate slow-wave brain activity reduce the presence of pathological molecules and preserves cognitive abilities in a rodent model of traumatic brain injury. Researchers are hopeful sleep modulation could serve as a viable treatment option after traumatic brain injury.
Traumatic brain injury (TBI) is an acquired injury to the brain that can cause cognitive impairment, comatose states, and death. Over 12% of the global population is affected by TBI and it is most commonly caused by falls, violence, and vehicular accidents. Diffuse damage to axons, which are projections that extend from neurons, contributes to post-TBI cognitive impairment and neurodegeneration. This axon damage is characterized by the increased presence of the pathological molecule amyloid precursor protein (APP). It has been proposed by scientists that sleep modulation interventions that enhance slow-wave brain activity, or deep sleep, can clear APP from the brain and reduce cognitive decline after TBI.
In a study recently published in the Journal of Neuroscience, researchers examined whether sleep restriction or sleep induction reduced axon damage and improved cognitive deficits in a rat model of TBI. TBI animals were separated into 3 experimental groups, 1) sleep restriction by gentle handling of the animal, 2) sleep induction by injection of a sleep-inducing drug, and 3) control with no intervention. All brain activity was monitored by implanted electrodes over the course of 5 days. After intervention, the cognitive abilities of the animals were evaluated based on a test for novel objects and their resulting exploratory behaviour. The extent of axon damage was evaluated histologically by the presence of APP.
It was discovered that control TBI animals with no intervention developed cognitive impairment and were unable to discriminate novel objects in the behaviour task. In contrast, it was observed that cognitive impairment was prevented in animals in the sleep restriction and sleep induction intervention groups, as their performance on the behaviour test was similar to baseline performance prior to trauma. Furthermore, less APP was seen in histological brain sections of animals exposed to both sleep intervention conditions compared to controls, suggesting that the interventions also prevented axon damage.
The researchers of this study hypothesize that sleep modulation immediately after TBI produces a deeper sleep, which has been proposed to be important for consolidating memories and clearing out noxious molecules like APP from the brain to reduce secondary injury and degeneration. However, further investigation is required to examine the mechanisms of slow-wave sleep in relation to trauma and how it can be utilized in practice for TBI and other neurological conditions for its neuroprotective effects.
Written By: Fiona Wong, PhD