Over 10 years we helping companies reach their financial and branding goals. Onum is a values-driven SEO agency dedicated.

CONTACTS
Traumatic Brain Injury Sleep Modulation

Acute Sleep Modulation and Traumatic Brain Injury Study

Sleep Modulation Alleviates Axonal Damage and Cognitive Decline after Rodent Traumatic Brain Injury

Marta Morawska, Fabian Buchele, Carlos Goncalves Moreira, Lukas L. Imbach, Daniela Noain, & Christian R. Baumann
Department of Neurology, University Hospital of Zurich, 8091 Zurich, Switzerland

Traumatic brain injury (TBI) is a major cause of death and disability worldwide. It produces diffuse axonal injury (DAI), which contributes to cognitive impairment, but effective disease-modifying treatment strategies are missing. We have recently developed a rat model of closed skull TBI that reproduces human TBI consequences, including DAI and clinical sequelae such as memory impairment. Here, we investigated whether sleep modulation after trauma has an impact on DAI and memory outcome. We assessed cognition with the novel object recognition test and stained for amyloid precursor protein, a DAI marker. We found that both sleep induction and restriction acutely after TBI enhanced encephalographic slow-wave activity, markedly reduced diffuse axonal damage in the cortex and hippocampus, and improved memory impairment 2 weeks after trauma. These results suggest that enhancing slow-wave sleep acutely after trauma may have a beneficial disease-modifying effect in subjects with acute TBI.

Traumatic Brain Injury Significance Statement

Traumatic brain injury (TBI) is a clinically important entity. Cognitive deficits belong to the most prevalent chronic posttraumatic symptoms, most likely due to diffuse axonal injury (DAI). A growing body of evidence suggests a role of sleep in the clearance of waste products in the brain, possibly including amyloid precursor protein (APP), a marker of DAI. In this study, we provide evidence that enhancement of slow-wave oscillatory activity in the delta-frequency range decreases the APP-immunoreactivity and preserves cognitive abilities after trauma, potentially offering novel, noninvasive treatment options for traumatic injury.

TBI Introduction

Traumatic brain injury (TBI) is a major public health concern affecting 12% of the general population worldwide and resulting in high rates of death and disability. The mostcommoncauses of TBI include violence, vehicle accidents, and falls (Styrke et al., 2007). TBI is currently interpreted as a disease process (Masel and DeWitt, 2010), presenting not only with acute manifestations, but also with long-lasting symptoms, potentially originated by progressive axonal injury (Bramlett and Dietrich, 2002, Inglese et al., 2005). Studies suggest that diffuse axonal injury (DAI) is an important contributor to posttraumatic cognitive impairment (Li et al., 2006, Kraus et al., 2007, Rostami et al., 2012), which is one of the most prevalent symptoms after TBI (Hall et al., 2005). Immunoreactivity to APP has been established as a gold standard for the detection of DAI. In addition to APP, pathological molecules that are linked to enhanced endoplasmic reticulum (ER) stress and to unfolded protein response, both of which are associated with neuronal death and with neurodegenerative disorders, have also been found to accumulate in the traumatized brain. Among these are activating transcription factor 4 (ATF-4), an ER stress marker, and ubiquitin (UB), a small regulatory protein playing a role in degradation of other proteins (Begum et al., 2014). Potentially noxious molecules are cleared via glymphatic pathways in the brain (Iliff et al., 2014, Plog et al., 2015), particularly during sleep and anesthesia, which are both characterized by predominant slow-wave activity (Xie et al., 2013). Indeed, there is an emerging discussion that sleep might serve as a potential treatment for a number of neurological conditions. Sleep restriction, resulting in increased slow-wave activity during subsequent rebound sleep (Borbe´ly et al., 1984, Franken et al., 1991), has been suggested to be beneficial for TBI (Martinez-Vargas et al., 2012) and stroke subjects (Cam et al., 2013). However, not only physiological sleep, but also pharmacological interventions aimed at increasing slow oscillatory encephalographic activity, were linked to APP clearance in an Alzheimer’s disease model (Klein et al., 2015) and similar interventions also improved outcome after stroke in rodents (Gao et al., 2008). Therefore, there is increasing evidence that interventions that enhance slow-wave activity could constitute novel, noninvasive treatment options for acute and chronic neurological conditions.

In this study, we aimed to assess whether sleep modulation procedures that induce increased slow-wave immediately after trauma improve diffuse axonal damage and TBI-induced cognitive deficits in a rat model of TBI.

To read the full Morawska acute sleep modulation and traumatic brain injury study, pleasebutton below to view or download the PDF file.

Barry Bruder

Barry Bruder

CEO & Founder of IASIS Technologies International

To share the IASIS Technologies International news article, click on the social media application of choice below.

Share on facebook
Share on twitter
Share on linkedin
Share on reddit
Share on email

Blog posts are not the opinion of IASIS Technologies International and its providers. No treatment for healing neurological conditions has been expressed or implied.

DISCLAIMER: This website does not contain medical advice. IASIS MCN is not a medical treatment, rather the retraining of the brain and nervous system. The information, including but not limited to text, videos, images and other material contained on this website is for informational purposes only. The purpose of this website is to promote broad consumer understanding and knowledge about IASIS MCN. It is not intended to be a substitute for professional medical advice, diagnosis or treatment. If you believe you have a medical condition, please first, always seek the advice of your physician or other qualified health care provider with any questions you may have regarding a medical condition or treatment and before undertaking a new health care regimen, and never disregard professional medical advice or delay in seeking it because of something you have read on this website. Video and written success stories contained on this site are the sole experience of those individuals shown or having written them, and are not the opinions of IASIS Technologies, Inc. Never self-medicate or choose to discontinue taking medicine without discussing your medical care with your doctor.

IASIS Technologies International

41951 Remington Ave STE 140

Our Address

info@iasistech.com

Our Mailbox

+1-951-972-3013

Our Phone

Copyright © 2021 IASIS Technologies International. All Rights Reserved.

Provider Registration

To gain access to the Provider section, new members must first purchase the IASIS Micro Current Neurofeedback System. Once you have the device in your possession with the system serial number, you can complete the registration form process below. The registration process can take 3-5 days for approval.

 
  • Please choose a username that has no spaces.

  • Silver MCN Provider Membership
 
  • Iasis Tech Log-in

    Provider Login

    Enter your username and password to access the many tools and resources for IASIS Micro Current Neurofeedback hardware and software.