CALBINDIN D-28K AND PARVALBUMIN IMMUNOREACTIVITY IN THE FRONTAL-CORTEX IN PATIENTS WITH FRONTAL-LOBE DEMENTIA OF NON-ALZHEIMER TYPE ASSOCIATED WITH AMYOTROPHIC-LATERAL-SCLEROSIS
CALBINDIN D-28K AND PARVALBUMIN IMMUNOREACTIVITY IN THE FRONTAL-CORTEX IN PATIENTS WITH FRONTAL-LOBE DEMENTIA OF NON-ALZHEIMER TYPE ASSOCIATED WITH AMYOTROPHIC-LATERAL-SCLEROSIS
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DOI：
10.1136/jnnp.56.3.257
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发表时间：
1993-03-01
影响因子：
11
通讯作者：
RIVERA, RM
中科院分区：
文献类型：
--
作者：
FERRER, I;TUNON, T;RIVERA, RM
用钙结合蛋白D-28K和小白蛋白免疫细胞化学方法，观察了2例非阿尔茨海默型额叶痴呆合并经典型肌萎缩侧索硬化症(ALS)患者和7例正常人额叶皮质(8区)局部环路神经元(中间神经元)的形态和分布。ALS患者Calbindin D-28k免疫反应细胞密度显著降低，但小白蛋白免疫反应神经元密度保持不变。在额叶痴呆患者中，主要位于皮质上层的Calbindin D-28K免疫反应神经元密度降低，可能干扰皮质-皮质联系的正常处理，而小白蛋白免疫反应细胞的完整性可能与保留主要的抑制性皮质内回路有关。
The morphology and distribution of local-circuit neurons (interneurons) were examined, by calbindin D-28k and parvalbumin immunocytochemistry, in the frontal cortex (area 8) in two patients with frontal lobe dementia of non-Alzheimer type associated with classical amyotrophic lateral sclerosis (ALS), and in seven normal cases. The density of calbindin D-28k immunoreactive cells was dramatically reduced in ALS patients, but the density of parvalbumin-immunoreactive neurons was preserved. Decreased density of calbindin D-28k-immunoreactive neurons, which are mainly located in the upper cortical layers, may interfere with the normal processing of cortico-cortical connections, whereas integrity of parvalbumin-immunoreactive cells may be associated with the preservation of the major inhibitory intracortical circuits in patients with frontal lobe dementia.