Wierzba-Bobrowicz Teresa, Lewandowska Eliza, Lechowicz Waldemar, Stepień Tomasz, Pasennik Elzbieta
Department of Neuropathology, Institute of Psychiatry and Neurology, Sobieskiego 9, 02-957 Warsaw, Poland.
Folia Neuropathol. 2005;43(2):81-9.
Under pathological conditions, microglial cells undergo activation, which is manifested by the expression of histocompatibility locus antigens class II (HLA II) on their surface as well as by proliferation and varied morphological forms. In schizophrenia, characterised by an essential role played by immunological mechanisms, quantitative analysis of activated microglia -- with well-developed ramification (RM), degenerative traits and damaged processes (from their shortening to their complete lack) (DM) -- may contribute to better understanding of schizophrenia etiopathogenesis. Quantitative analysis was performed on slices derived from the frontal and temporal lobes of 9 brains of schizophrenics and 6 control brains. The nonparametric Mann-Whitney U test was used to assess quantitative differences in the distribution of microglia in these regions of the brain. Statistical analyses were performed with STATISTICA 6.5 Programme. In both structures of the brain, the number of activated microglial cells was higher in schizophrenic brains than in control brains. Except for the first layer of the cerebral cortex with the same amounts of RM and DM, the number of DM cells in the remaining regions was several-fold higher than that of RM cells. It is most likely that disturbances in calcium metabolism and energetic balance as well as antibodies produced in the course of schizophrenia are the agents able to trigger a cascade transforming RM into DM. Quantitative differences in RM and DM, observed between the studied structures and cortical regions, could depend not only on functioning of inter-neuronal and inter-structural links. Our study suggests a pivotal role of microglial cells in repair processes and/or etiopathogenesis of schizophrenia and indicates that they undergo substantial damage in the course of chronic schizophrenia.
在病理条件下，小胶质细胞会发生激活，其表现为细胞表面表达组织相容性Ⅱ类抗原（HLAⅡ），以及细胞增殖和形态多样。精神分裂症的特征是免疫机制发挥重要作用，对具有发达分支（RM）、退行性特征和受损突起（从缩短到完全缺失）（DM）的活化小胶质细胞进行定量分析，可能有助于更好地理解精神分裂症的病因发病机制。对9例精神分裂症患者和6例对照者大脑额叶和颞叶切片进行了定量分析。采用非参数曼-惠特尼U检验评估大脑这些区域小胶质细胞分布的定量差异。使用STATISTICA 6.5程序进行统计分析。在大脑的两个结构中，精神分裂症患者大脑中活化小胶质细胞的数量均高于对照者大脑。除了大脑皮层第一层中RM和DM数量相同外，其余区域DM细胞的数量比RM细胞高出几倍。很可能是精神分裂症过程中钙代谢和能量平衡的紊乱以及产生的抗体能够引发将RM转化为DM的级联反应。在所研究的结构和皮层区域之间观察到的RM和DM的定量差异，可能不仅取决于神经元间和结构间联系的功能。我们的研究表明小胶质细胞在精神分裂症的修复过程和/或病因发病机制中起关键作用，并表明它们在慢性精神分裂症过程中受到严重损害。
