The contribution of demyelination to axonal loss in multiple sclerosis
The contribution of demyelination to axonal loss in multiple sclerosis
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DOI：
10.1093/brain/awl074
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发表时间：
2006-06-01
期刊：
影响因子：
14.5
通讯作者：
Esiri, M. M.
中科院分区：
文献类型：
--
作者：
DeLuca, G. C.;Williams, K.;Esiri, M. M.
多发性硬化是一种原发性脱髓鞘疾病的传统观念导致了以斑块为中心的病因学和疾病进展的发病机制的观点。轴突缺失的存在已得到越来越多的认识。然而，在多发性硬化症中脱髓鞘和轴突缺失的相对作用还没有完全阐明，也没有阐明它们之间可能的相互关系。对55名多发性硬化患者（29名男性）的大脑、脑干和脊髓的尸检材料进行髓鞘染色，年龄范围为25-83岁（平均= 57.5岁），病史长度范围为2 - 43年（平均= 17.1年）。通过将斑块面积与皮质脊髓和感觉束在每个水平的总白色物质面积相比的相对比例相加来计算斑块负荷。这与脊髓中这些神经束的轴突密度和轴突总数的估计有关。我们的研究结果表明，斑块负荷与脑重量无关。出乎意料的是，调整性别，年龄和病程后，总斑块负荷和轴突损失的皮质脊髓束和感觉束之间的相关性弱或不存在在每个级别的调查。由于斑块负荷和轴突损失之间的相关性很小，脱髓鞘不是脊髓轴突损失的主要决定因素的可能性值得考虑。
The traditional notion that multiple sclerosis is a primary demyelinating disease has led to a plaque-centred view of both aetiology and the pathogenesis of disease progression. The presence of axonal loss has received increasing recognition. However, the relative roles of demyelination and axonal loss have not been fully clarified in multiple sclerosis nor have their possible interrelationships been elucidated. Post-mortem material from the cerebrum, brainstem and spinal cord of 55 multiple sclerosis patients (29 males) with an age range of 25-83 years (mean = 57.5 years) and length of disease history ranging from 2 to 43 years (mean = 17.1 years) was stained for myelin. Plaque load was calculated by summing the relative proportion of plaque area compared with total white matter area of the corticospinal and sensory tracts at each level. This was related to estimates of axonal density and of total axon number in these tracts in the spinal cord. Our results indicate that plaque load did not correlate with brain weight. Unexpectedly, after adjusting for sex, age and duration of disease, correlations between total plaque load and axonal loss in both the corticospinal tract and sensory tracts were weak or absent at each level investigated. Since there was little correlation between plaque load and axonal loss, the possibility that demyelination is not the primary determinant of spinal cord axonal loss warrants consideration.