Ling Helen, Asi Yasmine T, Petrovic Igor N, Ahmed Zeshan, Prashanth L K, Hazrati Lili-Naz, Nishizawa Masatoyo, Ozawa Tetsutaro, Lang Anthony, Lees Andrew J, Revesz Tamas, Holton Janice L
Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UK.
Reta Lila Weston Institute of Neurological Studies, UCL Institute of Neurology, London, UK.
Mov Disord. 2015 Jun;30(7):960-7. doi: 10.1002/mds.26220. Epub 2015 Apr 8.
Glial cytoplasmic inclusions containing α-synuclein are the pathological hallmark of multiple system atrophy (MSA). Minimal change (MC-MSA) is an unusual MSA subtype with neuronal loss largely restricted to the substantia nigra and locus coeruleus.
Immunohistochemistry on selected brain regions and semiquantitative assessment were performed on six MC-MSA and eight MSA control cases.
More neuronal cytoplasmic inclusions were seen in the caudate and substantia nigra in MC-MSA than in MSA controls (P = 0.002), without any statistical difference in glial cytoplasmic inclusion load in any region. Severe glial cytoplasmic inclusion load was found in the ventrolateral medulla (P = 1.0) and nucleus raphe obscurus (P = 0.4) in both groups. When compared with MSA controls, the three MC-MSA cases who had died of sudden unexpected death had an earlier age of onset (mean: 38 vs. 57.6 y, P = 0.02), a numerically shorter disease duration (mean: 5.3 vs. 8 y, P = 0.2) and a more rapid clinical progression with most of the clinical milestones reached within 3 y of presentation, suggesting an aggressive variant of MSA. Another three MC-MSA cases, who had died of unrelated concurrent diseases, had an age of onset (mean: 57.7 y) and temporal course similar to controls, had less severe neuronal loss and gliosis in the medial and dorsolateral substantia nigra subregions (P < 0.05) than in MSA controls, and could be considered as a unique group with interrupted pathological progression. Significant respiratory dysfunction and early orthostatic hypotension were observed in all MC-MSA cases.
Our findings could suggest that α-synuclein-associated oligodendroglial pathology may lead to neuronal dysfunction sufficient to cause clinical symptoms before overt neuronal loss in MSA. © 2015 International Parkinson and Movement Disorder Society.
含有α-突触核蛋白的胶质细胞质内含物是多系统萎缩(MSA)的病理标志。微小病变型(MC-MSA)是一种不常见的MSA亚型,神经元丢失主要局限于黑质和蓝斑。
对6例MC-MSA病例和8例MSA对照病例的选定脑区进行免疫组织化学检测和半定量评估。
与MSA对照相比,MC-MSA的尾状核和黑质中可见更多神经元细胞质内含物(P = 0.002),而各区域胶质细胞质内含物负荷无统计学差异。两组的腹外侧延髓(P = 1.0)和中缝隐核(P = 0.4)中均发现严重的胶质细胞质内含物负荷。与MSA对照相比,3例死于意外猝死的MC-MSA病例起病年龄更早(平均:38岁对57.6岁,P = 0.02),病程在数值上更短(平均:5.3年对8年,P = 0.2),且临床进展更快,大多数临床里程碑在发病后3年内达到,提示为侵袭性MSA变异型。另外3例死于无关并发疾病的MC-MSA病例,起病年龄(平均:57.7岁)和病程与对照相似,内侧和背外侧黑质亚区域的神经元丢失和胶质增生程度比MSA对照轻(P < 0.05),可被视为病理进展中断的独特组。所有MC-MSA病例均观察到明显的呼吸功能障碍和早期体位性低血压。
我们的研究结果可能提示,α-突触核蛋白相关的少突胶质细胞病理可能导致神经元功能障碍,足以在MSA出现明显神经元丢失之前引起临床症状。© 2015国际帕金森病和运动障碍协会