Microglial are the resident macrophage of the central nervous system (CNS) parenchyma that participate in both CNS innate and adaptive immunity as well as taking part in many CNS development and homeostasis maintenance to support brain integrity. Credited to these roles, emerging evidence implicates microglial as key player that executing both beneficial and detrimental effects in various CNS-related neurological disease including neurodegeneration, neoplastic disease as well as neural development disorders.
Emerging evidence implicates microglial play critical roles to the CNS development of the brain. Microglial are unique population arise from immature yolk-sac macrophages that migrate and colonize the developing brain (Ginhoux et al., 2010; Ransohoff and Cardona, 2010). Interestingly, microglial (or their precursor cells) are selectively integrating into proliferative neurogenic zone of the proliferation and regulating the size of neural precursor cell pool via phagocytose neural precursor cell upon completion of neurogenesis(Cunningham et al., 2013). Also, colonization of microglia in the developing brain almost concurs temporally with brain vascularisation, neuroepithelial-radial glia transformation, neuronal migration, and myelination. Recent advent of transgenic technology and pharmacology allowed the role of microglia during development and their correlation with neural development disorder to be investigated extensively. For instance, pharmacologically knockout or inactivation of embryonic microglia resulted in increases of neural precursor cells pool (Cunningham et al., 2013). Similar phenomenons were also observed in genetically knockout of microglial in mice. Colony stimulating factor 1R-deficient (Csf1r−/−) mice w...
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.... Glioma-initiating cells: a predominant role in microglia/macrophages tropism to glioma. Journal of neuroimmunology 232, 75-82.
Zhan, Y., Paolicelli, R.C., Sforazzini, F., Weinhard, L., Bolasco, G., Pagani, F., Vyssotski, A.L., Bifone, A., Gozzi, A., Ragozzino, D., et al. (2014). Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior. Nature neuroscience 17, 400-406.
Zilka, N., Stozicka, Z., Kovac, A., Pilipcinec, E., Bugos, O., and Novak, M. (2009). Human misfolded truncated tau protein promotes activation of microglia and leukocyte infiltration in the transgenic rat model of tauopathy. Journal of neuroimmunology 209, 16-25.
Zoghbi, H.Y., and Bear, M.F. (2012). Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. Cold Spring Harbor perspectives in biology 4.
Microglia- act as part of the immune system, remove waste material and viruses and fungi from the brain
Around the world, many people are living with neurologically debilitating disorders like multiple sclerosis. Multiple sclerosis is best described as a pathological “inflammatory-mediated demyelinating disease of the human central nervous system,” and affects more than 2.5 million people globally (Trapp & Nave, 2008).
This is a disease is found in the brain and is caused by a buildup of a protein called tau. Tau slowly kills brain cells. Even after brain trauma has ended this process still continues. There are many symptoms such as memory loss, confusion, impaired judgement, depression, and even aggression.
“Guillain-Barre is an immune mediated response that triggers destruction of the myelin sheath covering the pe...
In the last 20 years ago, there was a brain scientists that believed that neurons communicated to each other, they represented thoughts, and that glia were kind of like a stucco and mortar holding the house together. They were also considered simple insulators for neuron communication. There is a few of types of glial cells, but recently scientists have begun to focus on a particular type of glial cell it is called the astrocyte; it’s an abundant in the cortex. As you go up the evolutionary ladder, astrocytes in the cortex increase in size and number, with humans having the most astrocytes and also the biggest. Scientists also discovered that astrocytes communicate to themselves in the cortex and they are also capable of sending information to neurons. Astrocytes are also the adult stem cell in the brain and control blood flow to regions of brain activity.
(Marieb, 2016). Myelin is the protective coat surrounding and insulating the nerve fibers of CNS. Myelin is fatty tissue substance that if attacked by immune cells causing a short-circuits in the current so that the successive gaps are excited more and more slowly, and eventually impulse conduction ceases which resulted in various forms of symptoms (Marieb, 2016). The degradation could either be “by inflammation, stroke, immune disorder, metabolic disorders, or nutritional deficiencies” (Slomski, 2005). The target that immune cells are sensitized to attack remains
Multiple sclerosis is a chronic inflammatory autoimmune disease of the central nervous system, directed against the myelin sheath. Leading to demyelination and axonal loss. It’s characterized by spread “plaques” of demielinization typically found in typically found on MRI in the periventricular region, corpus callosum, centrum semiovale and, to a lesser extent, deep white – structures and basal ganglia.(Olek, 2005)
... resulting impairment to the CNS. The first group of mice exhibited a pattern of CNS inflammation that resembled that of the most common subtype of MS, RRMS, with lesions filled with macrophages, a type of immune defender cell. The second group of mice displayed inflammation deep in the CNS tissues and in the optic nerve with lesions filled with neutrophils, another type of immune cell. Both groups of mice were given antibody drugs similar to drugs being developed against MS in humans. The effects were observed over time and results showed that some of the drugs inhibited disease in the first group of mice but did not inhibit disease in the second group. Thus, as Mark Kroenke (2008), the study’s first author and a Ph.D. student in immunology at U-M stated, "That's our proof that these really are different mechanisms of disease" (Kroenke et al., 2008).
...he activate local microglia.[63] Activated microglia can contribute to blood brain barrier opening.[64] Inflammation following blood brain barrier disruption after traumatic brain injury might be vital for the implementation of tissue repair and reorganization or even cell death.[65]
Multiple sclerosis was first discovered in 1868 by a neurologist by the name of Jean Martin- Charcot. Multiple sclerosis receives its name from the distinctive areas of scar tissue with the formation of damaged myelin sheaths. Multiple Sclerosis is referred to as an immune- mediated response that targets the central nervous system, including the spinal cord, the brain, and other parts of the body. The central nervous system is usually targeted by an abnormal response to the human body’s immune system causing an attack on the myelin coated fibers around nerve fibers. Generally, this occurs due to inflammation of myelin in the brain, causing lesions or plaques to form. Since myelin sheaths in the nervous system are there to increase nerve impulses,
Why does this self-inflicted deconstruction of the myelin occur? Multiple sclerosis is said to have genetic and environmental factors to its cause. Malnutrition and free radicals can all trigger a dormant M.S. gene in a person. According to the National Multiple Sclerosis Society, What Causes MS, studies say that “Growing evidence suggests that vitamin D plays an important role. People who live closer to the equator are exposed to greater amounts of sunlight year-round. As a result, they tend to have higher levels of naturally-produced vitamin D.” In fact, vitamin D holds specific immune strengthening qualities. Make it a priority to remain nourished, keeping your immune system at optimal strength, thus preventing pos...
John, L.R.; Morrow, Eric M.; Walsh, Christopher A. “Autism and Brain Development”. The Cell, 2008, 135:396–400.
Multiple Sclerosis is a demyelinating disease cause a widespread degeneration of the central nervous system (CNS) which gradually results in severe neurological deficits. The disease is characterized by remissions and relapse, erratic onset and duration is flare up acutely. Each relapse may involve different area in white matter in central nervous system (CNS) .
...areas, and creation of gitter cells (Gehrmann et al., 1995). Moreover, considering the importance of microglial, without microglial cells, the CNS will not survive (mortality) from external environment substance and pathogens. Thirdly, microglial cells are also responsible for homeostasis, negative and positive feedback loop, in CNS (Aloisi, 2001). Microglia is known for achieving complex communication via triggering signals molecules with other astrocytes, neural tissues, T lymphocytes and hematopoietic stem cells (Aloisi, 2001).
During early childhood, there is a huge proliferation of connections between neurons, usually peaking around the age of two. The adolescent brain then cuts down the amount of connections, deciding which ones are important to keep and which can be let go. While there are various theories as to the molecular mechanisms by which pruning actually occurs, most agree that pruning is primarily carried out by a very motile form of glial cell, called microglia [1], and pre-programmed cell death (apoptosis). These microglia are thought to remove cellular debris and perform surveillance during the healing process of an injured brain, but in the healthy, developing brain they have a possibly more important function. If a synapse receives little activity, it is weakened and eventually deleted by microglia and other glial cells through a process called long-term depotentiation (LTD). After the synapse has been removed, the space and resources that it once used are taken by other synapses. These synapses are strengthened by long-term potentiation (LTP). These processes and various others take place throughout development, peaking at adolescence and reaching their base around the age of 21, and transform the brain to create more complex and efficient neuronal configurations.