A scientist who is working to better understand the acceleration and whether interventions like cannabinoids can improve patient outcomes says that inflammation inside the brain can accelerate in the hours and days following a traumatic brain injury to the point where additional brain damage occurs.
According to Dr Kumar Vaibhav, a translational neuroscientist in the Department of Neurosurgery at the Medical College, "You cannot suppress the entire pro-inflammatory process, otherwise it would be difficult to recover from your injury. However, most TBI patients would benefit from therapy to create a better balance between the vigorous inflammation needed in the immediate aftermath to clean up the site and the deceleration needed to complete healing and avoid further brain damage".
While some TBI patients recover well, the majority would benefit from therapy to create However, excessive inflammation is to blame for the fact that one third of hospitalized TBI patients die from damage that persists after the initial injury.
Another example is the aftermath of concussions, which are injuries to the closed head that occur in football players. Headaches, dizziness, and fogginess are examples of immediate issues, but persistent memory and sleep issues, depression, epilepsy, and diseases like Alzheimer's and Parkinson's can also develop later.
Neither careful nor clinical mediation regularly empower control of irritation to restrict the optional obliteration, and better comprehension of irritation in the mind is a significant hindrance to effective treatment, the researcher says
Vaibhav is the principal investigator on a new $1-8 million grant (1RO1NS114560) from the National Institute of Neurological Disorders and Stroke that focuses on further investigating the function of the body's endocannabinoid system. This system was initially identified by researchers who were studying the mind-altering effects of THC, and it is now known to play a role in immunity, sleep, memory, and even reproduction. It appears that the physical damage to our brains initiates its involvement.
The plasma membrane of the injured brain cells, which helps keep the cell's contents contained, ruptures during a TBI, releasing lipids, or fats, a major membrane component, throughout the body. 2-AG and AEA, two important endocannabinoids that are also lipid molecules, are released from the damaged membrane where they are produced.
In order to assist in regulating the immune response, these molecules are supposed to bind with endocannabinoid receptors and activate the endocannabinoid system. CB2 receptors, which are found on immune cells and are known to reduce inflammation and related issues like swelling and blood vessel dysfunction, appear to be the 2-AG's target in this instance. CB1 and CB2 are the two main endocannabinoid receptors.
According to Vaibhav, we see CB2 receptor activation and expression go up within 24 hours after an injury, with 2-AG secreted in the blood. It is a quick response. The problem is that the damaged cells also release an enzyme called M-A G L, which is further activated by the now-free-floating lipids.
As its long name suggests, M-A G L, or enzyme lipase, is an enzyme whose function is to degrade 2-AG after it has completed its function. Vaibhav asserts that although activation of M-A G L is known to worsen TBI outcomes, the precise function it performs following TBI is unknown.
According to Vaibhav and his colleagues, the issue lies in the fact that high M-A G L appears to break down 2-AG before it can fulfill its crucial anti-inflammatory function. After a TBI, he proposes that elevated M-A G L levels instead function as a switch that raises inflammation. He also has some evidence that lowering M-A G L levels can assist in reestablishing a healthy synergy between M-A G L, 2-AG, and the CB2 cannabinoid receptor, making this a crucial intervention point.
To determine whether they are correct, his team is utilizing both a research drug that inhibits M-A G L and the cannabinoid CBD, of which they have early evidence that it also inhibits M-A G L
The team led by Vaibhav has discovered decreased 2-AG levels in the cerebrospinal fluid of TBI patients. Also, immune cells like macrophages are less likely to cause inflammation when they selectively activate the CB2 receptor early after a TBI. The objective is to determine the appropriate dosage and duration of the intervention so that it does not inhibit the aggressive immune response that is required to heal the injury
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