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Nerve cells interconnect through extensions called axons, which form a network within nerve fibers and the brain. These extend from the cell body, or soma, to ends where synapses relay electrical signals to other nerve cells. Axon degeneration can occur as a result of injury or disease. If the axon branch is severed, the separated segment usually breaks down, along with an attached section near the site of the break. Certain proteins may be involved in the axon degeneration process, but as of 2011 it is not known exactly which ones or how they proceed in breaking down cellular material.
When severed axons break down, this is called Wallerian degeneration. The process was first observed in the 1850s, but the sequence of events that trigger the process remain unclear. There also hasn’t been a general function that could be disrupted to stop axons from breaking down. Axon degeneration is typically influenced by three things: the internal dynamics of the cell, how the neuron reacts to an injury, and the molecular processes during degeneration.
The remaining section of axon on the cell usually degenerates a little after a break, but can survive. Changes in the nerve cell body enable fragments of the axon to be broken down. Branches of nerve cells can extend for thousands of times the diameter of the cell. Axons can be broken by being cut, crushed, or frozen, and chemical reactions can also damage them. Nerve cells can also undergo further deterioration following an injury when proteins are activated to respond to the initial damage.
Injuries and a variety of neurological diseases can lead to axon degeneration. Alzheimer’s Disease as well as Parkinson’s Disease can progress as many nerve cells lose their connections. Conditions such as diabetes and glaucoma often cause such physical effects on nerve cells as well. So can the neurological effects of chemotherapy. Injuries can involve direct impacts and other forces on nerve and brain tissue which can physically rip axons apart.
Researchers have found evidence that neurons can be internally programmed for axon degeneration. It is generally not known how this proceeds on a molecular level, but researchers have identified some of the proteins involved. By disrupting these proteins, degeneration because of chemotherapy has been delayed in studies. There is an ongoing search, as of 2011, to find a common method of axon degeneration so that medical treatments can prevent it in a variety of cases.
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