Plaques that form around the nerve cells of people with multiple sclerosis are apparently what disable people with the disease. But partly developed reparative cells within the plaques provide hope for a treatment, a UT Southwestern physician reports in the New England Journal of Medicine.
Dr. Elliot Frohman, professor of neurology and ophthalmology, is lead author on an overview of MS. It is the first time in five years that Journal editors have had researchers provide an overview of the debilitating disease.
Presently, the primary focus of research is on plaques, which are now known to contain certain predictable features consistent with tissue injury, such as loss of nerve insulation, scarring, inflammation and loss of the ability of nerves to transmit electrical and chemical information to other nerves.
"Recognizing these different injury cascades has catalyzed novel investigations into strategies for treatment that are aimed at promoting preservation of tissue architecture (neuroprotection) and even potentially neurorestoration," said Dr. Frohman, who directs the Multiple Sclerosis Program and Clinical Center at UT Southwestern and holds the Irene Wadel and Robert I. Atha Distinguished Chair in Neurology and the Kenney Marie Dixon-Pickens Distinguished Professorship in Multiple Sclerosis Research.
MS is an autoimmune disease in which the body attacks its own tissues and afflicts about 400,000 Americans and 2.5 million people worldwide. People with the disease develop problems with coordination and eyesight and, in some cases, lose mental sharpness.
In MS, nerve cells lose their insulating fatty covering, called myelin. Myelin comes from nearby cells called oligodendrocytes, which send out projections that wrap around nerve cells. Myelin allows electrical signals to travel quickly and with high fidelity.
The damaged area becomes surrounded by plaques, which contain a wide variety of cells. Although much of the content of a plaque is harmful to nerves, there are some cells that provide hope, Dr. Frohman said.
修复细胞疗法为治疗多重硬化症开辟了新的道路
核心摘要:
多发性硬化症的病理特征包括髓鞘破坏和神经功能障碍,伴随炎症和组织损伤。研究发现,残存的少突胶质细胞前体细胞(OPCs)在损伤区域具有潜在的修复能力,但其未成熟状态受抑制蛋白如Nogo和Lingo-1调控。激活OPCs促使其分化为成熟的少突胶质细胞,有望恢复髓鞘完整性,从而实现神经保护与再生。调控相关基因和蛋白的机制为多发性硬化症的细胞修复策略提供了新的治疗途径。