Neuroregeneration refers to the regrowth or repair of neural networks, cells, or cell products. Such mechanisms may include the formation of new neurons, glia, axons, myelin, or synapses. Neuroregeneration differs between peripheral nervous system (PNS) and central nervous system (CNS) by functional mechanism and especially level and speed. When the axon is damaged, the distal segment degenerates Wallerian, losing its mielin sheath. The proximal segment may die by apoptosis or undergo a chromatolytic reaction, which is an improvement effort. On CNS, synaptic tightening occurs when the glial leg process attacks the dead synapse.
Nervous system injuries affect more than 90,000 people each year. It is estimated that spinal injury alone affects 10,000 every year. As a result of the high incidence of neurological injury, neurological regeneration and repair, a subfield of neural network engineering, is a rapidly growing field dedicated to the discovery of new ways to restore nerve function after injury. The nervous system is divided into two parts: the central nervous system, which consists of the brain and spinal cord, and the peripheral nervous system, which consists of the cranial and spinal cord along with the associated ganglia. While the peripheral nervous system has intrinsic abilities for repair and regeneration, the central nervous system, for the most part, is unable to repair itself and regenerate. There is currently no treatment to restore human neural function after injury to the central nervous system. In addition, some attempts at nerve regrowth through the PNS-CNS transition have not been successful. There is not enough knowledge about regeneration in the central nervous system. In addition, although the peripheral nervous system has the ability to regenerate, much research still needs to be done to optimize the environment for maximum potential regrowth. Neuroregeneration is clinically important, as it is part of the pathogenesis of many diseases, including multiple sclerosis.
Video Neuroregeneration
Regenerasi sistem saraf perifer
Neuroregeneration in the peripheral nervous system (PNS) occurs at a significant level. Acacia shoots form at the proximal end and grow until they enter the distal stump. Growth of the sprouts is governed by the secreted chemotactic factor of Schwann cells (neurolemmocytes). Injury to the peripheral nervous system immediately led to the migration of phagocytes, Schwann cells, and macrophages to the lesion site to clear debris such as damaged tissue. When the neural axons are cut off, the ends still attached to the body of the cell are labeled proximal segments, while the other end is called the distal segment. After injury, the proximal end swells and degenerates backwards, but once the debris is cleared, it begins to grow the axon and the presence of a growth cone can be detected. The proximal axons are able to grow back as long as the body cells are intact, and they have made contact with Schwann cells in the endoneurial canal or tube. Levels of human axon growth can reach 1 mm/day on small nerves and 5 mm/day on large nerves. The distal segment, however, undergoes degrees of Wallerian within hours of injury; axon and myelin degenerate, but endoneurium persists. At the later regeneration stage, the remaining endoneurial tubes direct the growth of the axons back to the correct target. During the degeneration of Wallerian, Schwann cells grow in columns arranged along the endoneurial tube, creating a band BÃÆ'¼ngner (boB) that protects and retains the endoneurial ducts. Also, macrophage and Schwann cells release neurotrophic factors that promote regrowth.
Maps Neuroregeneration
Regeneration of the central nervous system
Unlike peripheral nervous system injury, central nervous system injury is not followed by extensive regeneration. This is limited by the inhibitory effect of the glial and extracellular environments. A hostile, non-permissive growth environment, in part, was created by myelin-associated migratory inhibitors, astrocytes, oligodendrocytes, oligodendrocyte precursors, and microglia. The environment in CNS, especially after trauma, negates the repair of myelin and neurons. Growth factors are not expressed or re-expressed; for example, less laminin extracellular matrix. Glial scar quickly forms, and glia actually produces factors that inhibit remyelination and axon repair; for example, NOGO and NI-35. The axons themselves also lose the potential for growth with age, due to decreased expression of GAP 43 among others.
Slower degeneration of the distal segment than occurs in the peripheral nervous system also contributes to the inhibitory environment because myelin inhibition and axonal debris are not cleaned rapidly. All of these factors contribute to the formation of what is known as a glia scar, which the axons can not grow. The proximal segment attempts to regenerate after injury, but its growth is hindered by the environment. It is important to note that the central nervous system axons have been shown to grow back in the permissive environment; Therefore, a major problem for axonal regeneration of the central nervous system is to traverse or eliminate the site of inhibitory lesions. Another problem is that the morphology and functional properties of central nervous system neurons are very complex, for this reason neurons can not be functionally replaced by any of the other types (LlinÃÆ'¡s law).
Inhibition of axonal regeneration
The formation of glas cell scars is induced after damage to the nervous system. In the central nervous system, this formation of glia scars significantly inhibits nerve regeneration, leading to loss of function. Several families of molecules are released that promote and encourage the formation of glia scars. For example, changing the growth factors B-1 and -2, interleukins, and cytokines play a role in scar formation initiation. The accumulation of reactive astrocytes at the site of injury and the rising regulation of molecules that inhibit the growth of neurites contribute to neuroregeneration failure. The upregulated molecule alters the composition of the extracellular matrix in a manner that has been shown to inhibit the proliferation of neurite growth. The formation of these scars involves several types of cells and the family of molecules.
Chondroitin sulfate proteoglycan
In response to the triggering factors of scarring, astrocytes regulate the production of chondroitin sulfate proteoglycans. Astrocytes are the dominant type of glia cells in the central nervous system that provide many functions including damage mitigation, repair, and the formation of glia scars. The RhoA Path is involved. Chondroitin sulfate proteoglycans (CSPGs) have been shown to be regulated in the central nervous system (CNS) after injury. Repeated glucuronic acid and galactosamine disaccharides, glycosaminoglycans (CS-GAG), are covalently combined with CSPG core proteins. CSPG has been shown to inhibit in vitro and in vivo regeneration, but the role that CSPG vs. CS-GAGs core protein has not been studied to date.
Sulfate Proteoglycans
Like chondroitin sulfate proteoglycans, the production of proteoglycan sulfate filtration (KSPG) is regulated in reactive astrocytes as part of the formation of glia scars. KSPG has also been shown to inhibit the proliferation of neurite growth, limiting nerve regeneration. The sulfate film, also called keratosulfate, is formed from repeated galactose disaccharide units and N-acetylglucosamines. This is also 6-sulfate. This sulphate is essential for the elongation of the sulfur wrinkle chain. A study was conducted using N-acetylglucosamine 6-O-sulfotransferase-1 mice. Wild-type mice showed significant regulation of mRNA expressing N-acetylglucosamine 6-O-sulfotransferase-1 at the site of cortical injury. However, in mice with deficiency of N-acetylglucosamine 6-O-sulfotransferase-1, the expression of sulfate strain decreased significantly when compared with wild-type rats. Similarly, the formation of glial scar was significantly reduced in N-acetylglucosamine 6-O-sulfotransferase-1 mice, and as a result, neuronal regeneration was less inhibited.
Other inhibiting factors
Proteins of oligodendritic or glial origin that affect neuroregeneration: NOGO protein families, especially Nogo-A, have been identified as retardation inhibitors on CNS, especially in autoimmune mediated demyelination, as found in Experimental Autoimmune Encephalomyelitis (EAE) and Multiple Sclerosis (MS). Nogo A works well through the amino-Nogo terminals through unknown receptors, or with the Nogo-66 ends via NgR1, p75, TROY or LINGO1. Rejects the outcome of this inhibitor in enhancing remielination, since it is involved in the RhoA pathway.
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Clinical care
Surgery
Surgery can be done if the peripheral nerves have been cut or divided. This is called peripheral nerve reconstruction. The injured nerve is identified and exposed so that normal neural tissue can be examined above and below the level of injury, usually by enlargement, using loupes or operating microscopes. If a large segment of the nerve is harmed, as can occur in a crush or stretching injury, the nerve will need to be exposed in a larger area. The injured nerve parts are removed. The cut nerve end is then carefully examined again using a very small stitch. Nerve repair should be covered by a healthy tissue, which can be as simple as covering the skin or may require a moving skin or muscle to provide a healthy crease over the nerves. The type of anesthetic used depends on the complexity of the injury. A surgical tourniquet is almost always used.
Prognosis
Expectations after improvement of peripheral nerve surgery are divided depending on several factors:
- Age : Nerve restoration after surgical repair mainly depends on the age of the patient. Young children can restore nerve function from close to normal. Conversely, patients over the age of 60 with nerve cuts in hand will hope to recover only a protective sensation; namely the ability to distinguish hot/cold or sharp/boring.
- Injury Mechanisms : Sharp injuries, such as knife wounds, only damage the very short nerve segments, allowing direct stitching. Conversely, nerves divided by stretching or crushing may be damaged by long segments. These nerve injuries are more difficult to treat and generally have worse outcomes. In addition, related injuries, such as injuries to bone, muscle and skin, can make nerve recovery more difficult.
- Injury rate : Once the nerve is repaired, the regenerating nerve endings should grow to its target. For example, the wounded nerve in the wrist that usually gives thumb sensation should grow to the tip of the thumb to give sensation. The return of function decreases with increasing distance at which the nerve must grow.
Autologous nerve imagery
Currently, autologous nerve grafting, or autograft nerves, is known as the gold standard for clinical care used to correct large lesions in the peripheral nervous system. It is important that the nerve is not repaired under pressure, which can occur if the cut ends are direadili in the gap. The nerve segment is taken from another part of the body (the donor site) and inserted into the lesion to provide an endoneial tube for axonal regeneration across the gap. However, this is not a perfect treatment; often the end result is only limited function recovery. Also, partial deinnervation is often experienced in donor sites, and some operations are needed to harvest the network and plant it.
If necessary, the nearest donor can be used to supply innervation to the lesion's nerve. Trauma to donors can be minimized by using a technique known as end to end repair. In this procedure, an epineurial window is created on the donor nerve and the proximal end of the lethargic nerve is sewn over the window. Regeneration axons are diverted to stumps. The efficacy of this technique depends in part on the degree of partial neurectomy performed on the donor, with increased degree of neurectomy thus increasing the regeneration of axons within the lesion's nerve, but with the consequence of increasing the deficit in the donor.
Some evidence suggests that local delivery of dissolved neurotrophic factors at the site of autologous nerve grafting can improve axon regeneration in the graft and help speed up the functional recovery of a disabled target. Other evidence suggests that gene therapy that induces expression of neurotropic factors within the target muscle itself can also help increase axon regeneration. Accelerating neuroregeneration and reinnervation of a denervated target is essential to reduce the likelihood of permanent paralysis due to muscle atrophy.
Allografts and xenografts
Variations on the nerve autograft include allograft and xenograft. In allografts, graft tissue is taken from other people, donors, and planted in the recipient. Xenografts involves taking donor tissue from other species. Allografts and xenografts have the same disadvantages as autografts, but in addition, tissue rejection of the immune response must also be taken into account. Often immunosuppression is necessary with this graft. Disease transmission is also a factor when introducing tissues from other people or animals. Overall, allografts and xenografts do not match the quality of results seen with autografts, but they are needed when there is a lack of autologous nervous tissue.
Nervous guidance channel
Due to the limited functionality received from autografts, the current gold standard for neuronal regeneration and repair, recent neural network engineering studies have focused on developing bioartificial neural guidance channels to guide axonal growth. Artificial neural channel formation is also known as entubulation because the nerve endings and the intervening gap are enclosed in a tube composed of biological or synthetic materials.
Immunization
The direction of the research is on the use of drugs targeting the protein inhibitors of remielination, or other inhibitors. Possible strategies include vaccination against this protein (active immunization), or treatment with pre-made antibodies (passive immunization). This strategy appears promising in animal models with experimental autoimmune encephalomyelitis (EAE), the MS model. Monoclonal antibodies have also been used against inhibitory factors such as NI-35 and NOGO.
See also
- Myelinogenesis
- Neural protection
- Research on spinal cord injury
- Wallerian degeneration
References
Source of the article : Wikipedia
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