This chapter summarizes data indicating that neuronal injury is an integral part of MS, and that loss of axons, den-drites, and neurons contributes to the irreversible functional impairment observed in affected individuals. Recent reports describe various aspects and potential mechanisms of neuronal injury in MS. Through different methods and use of various animal models, our understanding of neuropatho-logical mechanisms involved in the development of permanent symptoms during the disease course has increased. Several lines of evidence indicate that primary inflammatory demyelination underlies early axonal loss during RR-MS; however, this axonal loss is clinically silent. The transition from RR-MS to SP-MS has been suggested to occur when a threshold of axonal loss is reached, and the compensatory capacity of the CNS is surpassed, resulting in the subsequent development of permanent neurological symptoms. The level of inflammatory activity during RR-MS determines the rate of neurodegeneration and the point at which a patient is said to have SP-MS.
The inflammatory neurodegenerative disease concept of MS has several clinical implications. Surrogate markers of axonal loss are needed to monitor neurodegeneration. Early aggressive anti-inflammatory and immunomodulatory treatment should be provided to prevent and delay disability. Neuroprotective therapeutics should be developed for MS.
Finally, further elucidation of the molecular mechanisms behind axonal injury and their relation to disease stage in MS is essential for the development of novel therapeutic strategies.
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