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首页> 外文期刊>Journal of Alzheimer's disease: JAD >Additive microglia-mediated neuronal injury caused by amyloid-β and bacterial TLR agonists in murine neuron-microglia co-cultures quantified by an automated image analysis using cognition network technology
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Additive microglia-mediated neuronal injury caused by amyloid-β and bacterial TLR agonists in murine neuron-microglia co-cultures quantified by an automated image analysis using cognition network technology

机译：使用认知网络技术通过自动图像分析对鼠神经元-小胶质细胞共培养物中淀粉样蛋白-β和细菌TLR激动剂引起的小胶质细胞介导的神经元附加损伤

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摘要

Activated microglia is considered to be involved in the progression of Alzheimer's disease (AD). We investigated the effect of amyloid-β 1-40 (Aβ 40) and exogenous agonists of Toll-like receptor (TLR) 1/2 (Pam 3CSK 4) and TLR4 (LPS) on neurons in primary murine neuron-microglia co-cultures. Neuronal viability, assessed by quantifying the number of intact neuronal extensions and their crossings using a newly developed Definiens Cognition Network Technology-based method, was significantly decreased after treatment with Pam 3CSK 4, LPS, and Aβ 40. Combined treatment with Aβ 40 and Pam 3CSK 4 or LPS had an additive effect. Hence, in patients with AD, synergistic microglial activation by Aβ and bacterial products during infections might contribute to disease progression.
机译：活化的小胶质细胞被认为与阿尔茨海默氏病（AD）的进展有关。我们研究了淀粉样β1-40（Aβ40）和Toll样受体（TLR）1/2（Pam 3CSK 4）和TLR4（LPS）的外源激动剂对原代鼠神经元-小胶质细胞共培养物中神经元的影响。 。通过使用新开发的基于Definiens认知网络技术的方法量化完整神经元延伸及其交叉的数量来评估神经元生存力，在用Pam 3CSK 4，LPS和Aβ40治疗后，神经元活力显着下降。联合使用Aβ40和Pam治疗3CSK 4或LPS具有加和作用。因此，在AD患者中，感染期间Aβ和细菌产物的协同小胶质细胞活化可能有助于疾病进展。

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