Neuroinflammation

Neuroinflammation takes place when the central nervous system (CNS), which consists of the brain and spinal cord, undergoes an immune response. This may be due to microglial cell activation.

Neuroinflammation is thought to occur when immune cells from the body infiltrate the central nervous system (CNS) (links to CNS page), which consists of the brain and spinal cord. Infiltration of these immune cells can occur both when the brain is damaged and when there is infection in the body.

Microglia, the primary defense mechanisms for the CNS, activate in response to the immune cells and respond to repair the damage in the brain or fight the infection.

As microglia work to restore damaged tissues by activating T-cells leading to further inflammation. Consistent microglia activation and release of these cells lead to the chronic damage that perpetuate neuroinflammation.

Diseases Associated with Neuroinflammation
Neuroinflammation is a symptom of many diseases and thought to be a part of ME. Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis are illnesses where the brain experiences decline in structure and function, and also where it shows clear signs of neuroinflammation. Inflammation of the brain is linked to activated microglia, cytokine presence in the brain (Chen et al., 2016), and changes in the neurochemicals produced by the brain (Albrecht et al., 2016). These effects also occur in ME which is why researchers are searching to more strongly show neuroinflammation in these patients.

Viruses can cause to these symptoms to appear in each of the disease backgrounds because viruses can directly interact with neurons which may lead to a breakdown in neuronal health. This ultimately affects cognitive abilities and behaviors (Chen et al., 2016)

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?

Learn more

 * Wikipedia