Perry, V. Hugh (2005) Inflammation and axon degeneration. In, Multiple Sclerosis As A Neuronal Disease. Academic Press, pp. 241-253. (doi:10.1016/B978-012738761-1/50018-3).
Abstract
Axon injury is a significant part of multiple sclerosis (MS) pathology. Postmortem analysis shows that axon injury occurs early in the evolution of the plaque, and the degree of axon injury correlates with the intensity of the inflammatory response. Studies in animal models of MS show that axon injury also occurs in a number of these models. The transection of an axon by inflammatory cells and their products is an irreversible lesion and insights into the early stages of this process are needed. Furthermore, a spectrum of molecules secreted by inflammatory cells including T-cells, B-cells, and macrophages in an immunologically nonspecific manner may precipitate axon transection. These "molecular scissors" may act on the axon in a number of different ways. They may activate biochemical pathways, intrinsic to the axon, that lead to local auto destruction similar to programmed-cell-death, or apoptosis, of the cell body. Therapeutic interventions to target the molecules of destruction that are secreted by inflammatory cells that act as molecular scissors to precipitate axon transection are much needed.
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