El Saftawy Enas A, Amin Noha M, Sabry Rania M, El-Anwar Noha, Shash Rania Y, Elsebaie Eman H, Wassef Rita M
Medical Parasitology Department, Faculty of Medicine, Cairo University, Cairo, Egypt.
Armed Forces College of Medicine, Cairo, Egypt.
J Parasitol Res. 2020 Jul 30;2020:8859857. doi: 10.1155/2020/8859857. eCollection 2020.
Dementia is an ominous neurological disease. Scientists proposed a link between its occurrence and the presence of (. The long-term sequels of anti- premunition, chiefly dominated by TNF-, on the neurons and their receptors as the insulin-like growth factor-1 receptor (IGF-1R), which is tangled in cognition and synaptic plasticity, are still not clear. IGF-1R mediates its action via IGF-1, and its depletion is incorporated in the pathogenesis of dementia. The activated TNF- signaling pathway induces NF- that may induce or inhibit neurogenesis. This study speculates the potential impact of anti- immune response on the expression of IGF-1R in chronic cerebral toxoplasmosis. The distributive pattern of cysts was studied in association with TNF- serum levels, the in situ expression of NF-, and IGF-1R in mice using the low virulent ME-49 strain. There was an elevation of the TNF- serum level ( value ≤ 0.004) and significant upsurge in NF- whereas IGF-1R was of low abundance ( value < 0.05) compared to the controls. TNF- had a strong positive correlation with the intracerebral expression of NF- ( value ≈ 0.943, value ≈ 0.005) and a strong negative correlation to IGF-1R ( value -0.584 and -0.725 for area% and O.D., respectively). This activated TNF-/NF- keeps under control at the expense of IGF-1R expression, depriving neurons of the effect of IGF-1, the receptor's ligand. We therefore deduce that immunopathological reaction may be a road paver for developing dementia.
痴呆是一种严重的神经疾病。科学家提出其发病与（此处原文缺失相关内容）的存在之间存在联系。抗预免疫的长期后果，主要由肿瘤坏死因子-α（TNF-α）主导，对神经元及其受体（如参与认知和突触可塑性的胰岛素样生长因子-1受体（IGF-1R））的影响仍不清楚。IGF-1R通过IGF-1介导其作用，其缺失与痴呆的发病机制有关。激活的TNF-α信号通路诱导核因子-κB（NF-κB），后者可能诱导或抑制神经发生。本研究推测抗免疫反应对慢性脑弓形虫病中IGF-1R表达的潜在影响。使用低毒力的ME-49株研究小鼠囊肿的分布模式与TNF-α血清水平、NF-κB的原位表达以及IGF-1R的关系。与对照组相比，TNF-α血清水平升高（P值≤0.004），NF-κB显著升高，而IGF-1R丰度较低（P值<0.05）。TNF-α与NF-κB的脑内表达呈强正相关（P值≈0.943，P值≈0.005），与IGF-1R呈强负相关（面积百分比和光密度的P值分别为-0.584和-0.725）。这种激活的TNF-α/NF-κB以牺牲IGF-1R表达为代价控制（此处原文缺失相关内容），使神经元无法获得受体配体IGF-1的作用。因此，我们推断（此处原文缺失相关内容）免疫病理反应可能是痴呆发展的铺路石。
