Potential for CBD to treat traumatic brain injuries, review concludes

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Cannabidiol (CBD) shows strong potential for its inclusion in clinical treatment of traumatic brain injuries (TBI), with mechanisms of action including the mediation of the cellular and biochemical changes associated with the injuries, a recent literature review concludes.

Collated evidence noted the abilities of CBD to mediate neurotransmitter regulation, prevent blood brain barrier (BBB) permeability, and decrease both reactive oxygen and nitrogen species (ROS/RNS) and microglial inflammatory responses.

As a result, CBD has been found to reduce neuroinflammation and act as a neuroprotectant, enabling for the reduction of associated cognitive and physiological symptoms of TBI.

“There is strong mechanistic support that CBD could be an effective pharmacological intervention for TBIs”, the researchers from Western Washington University conclude.

“There are currently no known blinded and randomized human clinical trials for CBD's neuroprotective effects in TBI, however, an upcoming phase II clinical trial will investigate the effects of CBD with or without 9-THC in patients with TBI,” they add.

CBD interest

The interest in CBD has grown rapidly in recent years, following observations highlighting anti-inflammatory, antioxidative and antiepileptic potentials.

As a result of these neuroprotective properties, there has been an increased interest in CBD’s use in therapeutic treatment for traumatic brain injury (TBI) to prevent against the secondary injury cascade; a vital stage to target following primary injury to prevent long-term health complications.

The complexities and variations in severity associated with TBI has created a lack of a single, effective pharmacological treatment. Yet, the noted effects on CBD on neurotransmitters, the blood brain barrier, and oxidative stress mechanisms have created strong potential for the use of CBD at this stage of TBI.

Following this, the researchers conducted a review to summarise the cascade effects triggered by TBI and the potential for CBD to counteract such outcomes.

The review

Based on the collated evidence, it was noted that CBD administration significantly mediated neurotransmitters, restored electron/ion balance, prevented BBB permeability, and decreased both microglial inflammation as well as ROS/RNS responses. This was achieved following the activation of cannabinoid receptors type 1 (CB1R) and 2 (CB2R).

Additionally, CBD was able to regulate calcium homeostasis, reduce neuroinflammation and protect against neurological damage. As a result, TBI-associated negative cognitive changes, in areas such as memory, attention, and mood, appeared to reduce.

The researchers highlight the importance of identifying effective dosage quantities that are consistent, due to the many competing mechanisms identified. In addition, gender-based differences were observed to potentially impact CBD’s effects.

Future potential

Many of the available evidence was collated from animal-based studies, highlighting the need for further RCTs to prove cause and effect responses in human cohorts. Yet, the review provides an important insight into the potential for the use of CBD for TBI.

“Current studies of CBD's effects on TBI suggest that CBD dosing and achieved concentrations are critical for achieving therapeutic benefits. Other characteristics such as method of administration, duration of exposure, and temporal proximity to the TBI further complicate efforts for achieving a clear understanding of optimal therapeutic strategies.

“Beyond dosing, sex-based differences in the ECS expression, cannabinoid metabolism, and energy homeostasis regulation may impact CBD's effects, and thereby, highlight the need for further investigation into biological sex and hormone-based differences in the response to CBD,” the researchers add.

 

Source: Frontiers in Nutrition

https://doi.org/10.3389/fneur.2023.1087011

“Cannabidiol's neuroprotective properties and potential treatment of traumatic brain injuries”

Mackenzie M. Aychman, David L. Goldman and Joshua S. Kaplan