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Axonal damage revealed by accumulation of beta-amyloid precursor protein in HTLV-I-associated myelopathy.




 

J Neurol Sci. 2000 Jun 15;176(2):95-101. Unique Identifier : AIDSLINE

We investigated the localization and extent of beta-amyloid precursor protein (APP) immunoreactivity as a sensitive marker for impairment of fast axonal transport in the spinal cords of patients with HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP). The results from this study show that APP, used as a marker of early axonal damage in HAM/TSP lesions, is more intensively expressed in areas of active-inflammatory lesions than those of inactive-chronic lesions. The close localization to the areas containing inflammation (activation of macrophage/microglia) is striking and suggests that axonal damage is closely associated with inflammation in active-chronic lesions. Although inflammatory cell infiltration in the central nervous system (CNS) is rarely found in inactive-chronic lesions, a few clusters of APP+ axons are found in the spinal cord white matter in some cases. The presence of APP+ axons without relation to inflammatory cells in inactive-chronic lesions, suggest that soluble neurotoxic factors might induce axonal changes in the CNS of HAM/TSP. The occasional myelinated fibers in the anterior and posterior spinal roots in lower thoracic to lumbar levels had APP+ axons, suggesting that spinal nerve roots can be affected in HAM/TSP, especially in lower thoracic to lumbar levels. Impairment of fast axonal transport may contribute to the development of disability in patients with HAM/TSP.

JOURNAL ARTICLE Aged Amyloid beta-Protein Precursor/*ANALYSIS Axonal Transport/PHYSIOLOGY Biological Markers Female Human Immunohistochemistry Male Middle Age Nerve Degeneration/*PATHOLOGY/PHYSIOPATHOLOGY Paraparesis, Tropical Spastic/*PATHOLOGY/PHYSIOPATHOLOGY Spinal Cord/PATHOLOGY/PHYSIOPATHOLOGY Support, Non-U.S. Gov't



 




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