感染Chlamydia pneumoniae和SARS-CoV-2以及阿尔茨海默氏病的病原发生
Alexa Romanella1, Maegan McCall2, Rachel Corwin1
1Department of Bio-Medical Sciences, Center for Chronic Disorders of Aging, Philadelphia College of Osteopathic Medicine (PCOM), Philadelphia, PA, United States.
某些传染病原体,如克拉米迪亚肺炎 (Cpn) 和SARS-CoV-2,可能会启动阿尔茨海默氏病 (AD) 的发病. 这些病原体可以进入大脑,引发神经炎症,并且与遗传风险因素如APOEε4.4有关.
科学领域:
- 神经科学是一个神经科学.
- 传染性疾病 传染性疾病
- 遗传学 遗传学 是一个
背景情况:
- 阿尔茨海默病 (AD) 是一种主要的神经退行性疾病,其原因尚不清楚.
- 新出现的证据表明,传染病原体可能在阿尔茨海默病发病过程中发挥作用.
- 冠状病毒肺炎 (Cpn) 和SARS-CoV-2都与阿尔茨海默病的发展有关.
研究的目的:
- 审查关于CPN,SARS-CoV-2和AD之间的关联的同行评审研究.
- 检查遗传风险因素,包括APOEε4,以及IL-6,CCL2和NRP1.1等生物标志物.
- 了解AD中感染和神经炎症的机制.
主要方法:
- 原始研究和评论文章的文献综述.
- 专注于CPN和SARS-CoV-2感染途径进入大脑.
- 对遗传风险 (APOEε4) 和炎症生物标志物的分析 (IL-6,CCL2,NRP1).
主要成果:
- 无论是CPN还是SARS-CoV-2,都可以通过嗅觉系统或血液进入大脑.
- 感染引发神经炎症,以增加IL-6和CCL2水平为标志.
- APOEε4表达增加了对CPN和SARS-CoV-2感染的易感性.
结论:
- 肺炎和SARS-CoV-2是通过神经炎症导致AD病变的潜在贡献者.
- 对于CPN (硫硫酸蛋白质糖) 和SARS-CoV-2 (ACE2受体,NRP1) 存在不同的进入机制.
- 需要进一步的研究来澄清因果关系和诊断潜力.
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