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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.[1]

Evidence[edit | edit source]

Immune and Brain Interaction[edit | edit source]

Research has shown that the brain and the immune system communicate through the vagus nerve[2]. , 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[3]. 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[2].

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[4]. Continued activation of this pathway could cause dysfunction leading to symptoms present in chronic fatigue syndrome, including neuroinflammation[5].

Causes[edit | edit source]

Oxidative and Nitrosative Stress[edit | edit source]

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). [6]

Notable studies[edit | edit source]

  • Autopsies of four deceased ME patients showed various pathological phenomena in the central and peripheral nervous systems. [7]
  • Brain Scans of ME/CFS from Stanford ME/CFS Initiative show inflammation. The New York Times article "Brains of People With Chronic Fatigue Syndrome Offer Clues About Disorder" has startling color images.[8]

Talks & interviews[edit | edit source]

Learn more[edit | edit source]

See also[edit | edit source]

References[edit | edit source]

  1. Graeber, M. B., Li, W., & Rodriguez, M. L. (2011). Role of microglia in CNS inflammation. FEBS letters, 585(23), 3798-3805.
  2. 2.0 2.1 Goehler, L. E., Relton, J. K., Dripps, D., Kiechle, R., Tartaglia, N., Maier, S. F., & Watkins, L. R. (1997). Vagal paraganglia bind biotinylated interleukin-1 receptor antagonist: a possible mechanism for immune-to-brain communication. Brain research bulletin, 43(3), 357-364
  4. Ren, K., and Dubner, R. (2008). Neuron-glia crosstalk gets serious: role in pain hypersensitivity. Curr. Opin. Anaesthesiol. 21, 570–579.
  5. VanElzakker, M. B. (2013). Chronic fatigue syndrome from vagus nerve infection: a psychoneuroimmunological hypothesis. Medical hypotheses, 81(3), 414-423.
  6. Morris, G., and Maes, M. (2014). Oxidative and nitrosative stress and immune-inflammatory pathways in patients with myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS). Current neuropharmacology, 12(2), 168-185.
  7. Pathology of CFS: Pilot Study of Four Autopsy Cases - Dec. 2010
  8. Brains of People With Chronic Fatigue Syndrome Offer Clues About Disorder

The information provided at this site is not intended to diagnose or treat any illness.

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history