Related Research Articles
Transverse myelitis (TM) is a rare neurological condition wherein the spinal cord is inflamed. The adjective transverse implies that the spinal inflammation (myelitis) extends horizontally throughout the cross section of the spinal cord; the terms partial transverse myelitis and partial myelitis are sometimes used to specify inflammation that affects only part of the width of the spinal cord. TM is characterized by weakness and numbness of the limbs, deficits in sensation and motor skills, dysfunctional urethral and anal sphincter activities, and dysfunction of the autonomic nervous system that can lead to episodes of high blood pressure. Signs and symptoms vary according to the affected level of the spinal cord. The underlying cause of TM is unknown. The spinal cord inflammation seen in TM has been associated with various infections, immune system disorders, or damage to nerve fibers, by loss of myelin. As opposed to leukomyelitis which affects only the white matter, it affects the entire cross-section of the spinal cord. Decreased electrical conductivity in the nervous system can result.
Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.
Myelitis is inflammation of the spinal cord which can disrupt the normal responses from the brain to the rest of the body, and from the rest of the body to the brain. Inflammation in the spinal cord can cause the myelin and axon to be damaged resulting in symptoms such as paralysis and sensory loss. Myelitis is classified to several categories depending on the area or the cause of the lesion; however, any inflammatory attack on the spinal cord is often referred to as transverse myelitis.
Pathophysiology is a branch of study, at the intersection of pathology and physiology, concerning disordered physiological processes that cause, result from, or are otherwise associated with a disease or injury. Pathology is the medical discipline that describes conditions typically observed during a disease state, whereas physiology is the biological discipline that describes processes or mechanisms operating within an organism. Pathology describes the abnormal or undesired condition, whereas pathophysiology seeks to explain the functional changes that are occurring within an individual due to a disease or pathologic state.
Neuromyelitis optica spectrum disorders (NMOSD), including neuromyelitis optica (NMO), are autoimmune diseases characterized by acute inflammation of the optic nerve and the spinal cord (myelitis). Episodes of ON and myelitis can be simultaneous or successive. A relapsing disease course is common, especially in untreated patients. In more than 80% of cases, NMO is caused by immunoglobulin G autoantibodies to aquaporin 4 (anti-AQP4), the most abundant water channel protein in the central nervous system. A subset of anti-AQP4-negative cases is associated with antibodies against myelin oligodendrocyte glycoprotein (anti-MOG). Rarely, NMO may occur in the context of other autoimmune diseases or infectious diseases. In some cases, the etiology remains unknown.
Neuroimmunology is a field combining neuroscience, the study of the nervous system, and immunology, the study of the immune system. Neuroimmunologists seek to better understand the interactions of these two complex systems during development, homeostasis, and response to injuries. A long-term goal of this rapidly developing research area is to further develop our understanding of the pathology of certain neurological diseases, some of which have no clear etiology. In doing so, neuroimmunology contributes to development of new pharmacological treatments for several neurological conditions. Many types of interactions involve both the nervous and immune systems including the physiological functioning of the two systems in health and disease, malfunction of either and or both systems that leads to disorders, and the physical, chemical, and environmental stressors that affect the two systems on a daily basis.
The neuroimmune system is a system of structures and processes involving the biochemical and electrophysiological interactions between the nervous system and immune system which protect neurons from pathogens. It serves to protect neurons against disease by maintaining selectively permeable barriers, mediating neuroinflammation and wound healing in damaged neurons, and mobilizing host defenses against pathogens.
Multiple sclerosis is an inflammatory demyelinating disease of the CNS in which activated immune cells invade the central nervous system and cause inflammation, neurodegeneration, and tissue damage. The underlying cause is currently unknown. Current research in neuropathology, neuroimmunology, neurobiology, and neuroimaging, together with clinical neurology, provide support for the notion that MS is not a single disease but rather a spectrum.
The kynurenine pathway is a metabolic pathway leading to the production of nicotinamide adenine dinucleotide (NAD+). Metabolites involved in the kynurenine pathway include tryptophan, kynurenine, kynurenic acid, xanthurenic acid, quinolinic acid, and 3-hydroxykynurenine. The kynurenine pathway is responsible for total catabolization of tryptophan about 95%. Disruption in the pathway is associated with certain genetic and psychiatric disorders.
Theiler's murine encephalomyelitis virus (TMEV) is a single-stranded RNA murine cardiovirus from the family Picornaviridae. It has been used as a mouse model for studying virally induced paralysis, as well as encephalomyelitis comparable to multiple sclerosis. Depending on the mouse and viral strain, viral pathogenesis can range from negligible, to chronic or acute encephalomyelitis.
Research indicates that living in areas of high pollution has serious long term health effects. Living in these areas during childhood and adolescence can lead to diminished mental capacity and an increased risk of brain damage. People of all ages who live in high pollution areas for extended periods place themselves at increased risk of various neurological disorders. Both air pollution and heavy metal pollution have been implicated as having negative effects on central nervous system (CNS) functionality. The ability of pollutants to affect the neurophysiology of individuals after the structure of the CNS has become mostly stabilized is an example of negative neuroplasticity.
Paul Ashwood is an associate professor of immunology at the MIND Institute at the University of California Davis. His lab conducts research regarding the potential role of immune system disorders in autism, as well as other neurodevelopmental disorders such as Fragile X syndrome, Tourette syndrome, schizophrenia and mood disorders.
Neuroinflammation is inflammation of the nervous tissue. It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity. In the central nervous system (CNS), including the brain and spinal cord, microglia are the resident innate immune cells that are activated in response to these cues. The CNS is typically an immunologically privileged site because peripheral immune cells are generally blocked by the blood–brain barrier (BBB), a specialized structure composed of astrocytes and endothelial cells. However, circulating peripheral immune cells may surpass a compromised BBB and encounter neurons and glial cells expressing major histocompatibility complex molecules, perpetuating the immune response. Although the response is initiated to protect the central nervous system from the infectious agent, the effect may be toxic and widespread inflammation as well as further migration of leukocytes through the blood–brain barrier may occur.
MOG antibody disease (MOGAD) or MOG antibody-associated encephalomyelitis (MOG-EM) is an inflammatory demyelinating disease of the central nervous system. Serum anti-myelin oligodendrocyte glycoprotein antibodies are present in up to half of patients with an acquired demyelinating syndrome and have been described in association with a range of phenotypic presentations, including acute disseminated encephalomyelitis, optic neuritis, transverse myelitis, and neuromyelitis optica.
Microglia are the primary immune cells of the central nervous system, similar to peripheral macrophages. They respond to pathogens and injury by changing morphology and migrating to the site of infection/injury, where they destroy pathogens and remove damaged cells.
Katerina Akassoglou is a neuroimmunologist who is a Senior Investigator and Director of In Vivo Imaging Research at the Gladstone Institutes. Akassoglou holds faculty positions as a Professor of Neurology at the University of California, San Francisco. Akassoglou has pioneered investigations of blood-brain barrier integrity and development of neurological diseases. She found that compromised blood-brain barrier integrity leads to fibrinogen leakage into the brain inducing neurodegeneration. Akassoglou is internationally recognized for her scientific discoveries.
Malú G. Tansey is an American Physiologist and Neuroscientist as well as the Director of the Center for Translational Research in Neurodegenerative Disease at the University of Florida. Tansey holds the titles of Evelyn F. and William L. McKnight Brain Investigator and Norman Fixel Institute for Neurological Diseases Investigator. As the principal investigator of the Tansey Lab, Tansey guides a research program centered around investigating the role of neuroimmune interactions in the development and progression of neurodegenerative and neuropsychiatric disease. Tansey's work is primarily focused on exploring the cellular and molecular basis of peripheral and central inflammation in the pathology of age-related neurodegenerative diseases like Alzheimer's disease and amyotrophic lateral sclerosis.
Amanda Brown is an American immunologist and microbiologist as well as an associate professor of neurology and neuroscience at Johns Hopkins University School of Medicine in Baltimore, Maryland. Brown is notable for cloning one of the first recombinant HIV viruses and developing a novel method to visualize HIV infected cells using GFP fluorescence.
There is increasing evidence suggesting that COVID-19 causes both acute and chronic neurologicalor psychological symptoms. Caregivers of COVID-19 patients also show a higher than average prevalence of mental health concerns. These symptoms result from multiple different factors.
The pathophysiology of autism is the study of the physiological processes that cause or are otherwise associated with autism spectrum disorders.
References
- ↑ Mealy, Maureen (January 2011). "The Johns Hopkins Transverse Myelitis Center: One Decade of Work and the Challenges for the Future". TMA. Retrieved 10 October 2013.
- ↑ Vargas, D. L.; Nascimbene, C.; Krishnan, C.; Zimmerman, A. W.; Pardo, C. A. (2005). "Neuroglial activation and neuroinflammation in the brain of patients with autism". Annals of Neurology. 57 (1): 67–81. CiteSeerX 10.1.1.512.6671 . doi:10.1002/ana.20315. PMID 15546155. S2CID 777608.
- ↑ Greenberg, David (15 November 2004). "Brain inflammation found in autism". Eurekalert! . Retrieved 10 October 2013.
- ↑ Blakeslee, Sandra (8 February 2005). "Focus Narrows in Search for Autism's Cause". The New York Times . Retrieved 10 October 2013.
- ↑ "Carlos A. Pardo-Villazimar". Johns Hopkins School of Medicine . Retrieved 10 October 2013.
- ↑ Tsouderos, Trine (23 November 2009). "Autism treatment: Science hijacked to support alternative therapies". Chicago Tribune . Retrieved 10 October 2013.
- ↑ "Brain's Immune System Triggered In Autism". ScienceDaily . 17 November 2004. Retrieved 10 October 2013.
- ↑ "Brain inflammation link to autism". BBC News . 15 November 2004. Retrieved 11 October 2013.