Mechanisms of injury-induced axon degeneration.

08:00 EDT 6th May 2019 | BioPortfolio

Summary of "Mechanisms of injury-induced axon degeneration."

Injury-induced axon degeneration in model organisms and cell culture has emerged as an area of growing interest due to its experimental tractability and to the promise of identifying conserved mechanisms that mediate axon loss in human disease. Injury-induced axon degeneration is also observed within the well-studied process of Wallerian degeneration, a complex phenomenon triggered by axon injury to peripheral nerves in mammals. Recent studies have led to the identification of key molecular components of injury-induced axon degeneration. Axon survival factors, such as NMNAT2, act to protect injured axons from degeneration. By contrast, factors such as SARM1, MAPK, and PHR1 act to promote degeneration. The coordinated activity of these factors determines axon fate after injury. Since axon loss is an early feature of neurodegenerative diseases, it is possible that understanding the molecular mechanism of injury-induced degeneration will lead to new treatments for axon loss in neurodegenerative disease. Here, we discuss the critical pathways for injury-induced axon degeneration across species with an emphasis on their interactions in an integrated signaling network.


Journal Details

This article was published in the following journal.

Name: Current opinion in neurobiology
ISSN: 1873-6882
Pages: 171-178


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Medical and Biotech [MESH] Definitions

Degeneration of distal aspects of a nerve axon following injury to the cell body or proximal portion of the axon. The process is characterized by fragmentation of the axon and its MYELIN SHEATH.

First segment of axon that connects distal axon segments to the neuronal CELL BODY at the axon hillock region. The axon initial segment is not protected by the MYELIN SHEATH and has properties critical for axonal growth. The axon initial segment and the axon hillock form an axonal trigger zone.

Prolonged unconsciousness from which the individual cannot be aroused, associated with traumatic injuries to the BRAIN. This may be defined as unconsciousness persisting for 6 hours or longer. Coma results from injury to both cerebral hemispheres or the RETICULAR FORMATION of the BRAIN STEM. Contributing mechanisms include DIFFUSE AXONAL INJURY and BRAIN EDEMA. (From J Neurotrauma 1997 Oct;14(10):699-713)

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The pathological mechanisms and forms taken by tissue during degeneration into a neoplasm and its subsequent activity.

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