Neuroinflammation



A concrete definition for neuroinflammation is not fully agreed on in the scientific world yet, but it is thought to follow similar patterns that inflammation in the rest of the body follows. Inflammation, in general, occurs when a pathogen, or something foreign to the body, gets into the body. The body detects the toxin with immune cells which then signal other immune cells to help eliminate the pathogen. The response and build-up of these immune cells is what is referred to as inflammation. The central nervous system (brain and spinal cord; CNS) are believed to do the same sort action with different types of cells. One of the main immune cells in the CNS is microglia, a type of brain cell that, when activated, signals other immune cells to help the brain fight diseases. This action is similar to how the body fights infection. Therefore, neuroinflammation is described as a combination of microglial activation and its response.

Immune and Brain Interaction
Research has shown that the brain and the immune system communicate through the vagus nerve. , a highly branched nerve that controls several systems of the body including sensory information to and from the heart, lungs and stomach, muscle movement including speech, homeostatic control of the heart, lungs and stomach, in addition to its effects in the immune system. When the body is infected by a foreign substance such as bacteria or a virus, the blood has sensors called macrophages floating around to detect the contaminate. The macrophages release the protein interleukin 1 beta (IL-1B) to start signaling the brain that there is a contagion present. This protein attaches to nearby vagus nerve protein receptors and upon connection, the vagus nerve alerts the brain to begin fighting off the bacteria or virus at this location. Activation of the vagus nerve in this manner causes the body to experience typical behaviors of a sick person such as sensitivity to pain stimuli, decreased appetite, and fever, all of which are regulated by the nerve.

Signaling along the vagus nerve pathway does not occur in isolation; when the nerve is firing in the brain, other neuronal cells also start to function in coordination. Glia, a different type of brain cell that lie adjacent to nerves and neurons in the brain, also becomes activated. The problem with activating the glial is that it can also trigger more cells to start functioning. Continued activation of this pathway could cause dysfunction leading to symptoms present in chronic fatigue syndrome, including neuroinflammation.

Oxidative and Nitrosative Stress
One possible for what may cause the inflamed cells in the brain follows a oxygen and nitrogen molecules. An overabundance of oxygen and nitrogen molecules in tissues can cause oxidative and nitrosative stress. The build-up causes negative chemical reaction between the tissues and the molecules leading to tissue damage. This relates to neuroinflammation because researchers propose a link between the dysfunction of brain tissues in ME/CFS and the breakdown of the oxidative and nitrosative stress pathway. This pathway helps maintain the blood-brain barrier, an important membrane keeping the brain protected from harmful substances present in the blood. When the pathway is dysfunctional, the blood-brain barrier becomes less effective at keeping out particles. This loss of efficacy could lead to immune cells entering the brain and beginning an immune response that leads to inflammation (e.g. neuroinflammation).

Notable studies

 * 2010, Autopsies of four deceased ME patients showed various pathological phenomena in the central and peripheral nervous systems.
 * 2014, Brains of People With Chronic Fatigue Syndrome Offer Clues About Disorder'. NY Times Well article by David Tuller on the brain scans of ME/CFS patient's researched by Stanford ME/CFS Initiative. (2014)

Talks & interviews

 * 2016, Do you have a hot brain?
 * 2016, What is neuroinflammation? (Jarred Younger)

Learn more

 * Wikipedia - Neuroinflammation