Studies have shown that the calcium ion (Ca²⁺) plays important roles both in Alzheimer’s dementia and SARS-CoV S-mediated fusion to host cell entry. An elevated level of intracellular calcium causes neuronal dysfunction, cell death, and apoptosis. Dysregulation of calcium has also been shown to increase the production of amyloid beta (Aβ) protein, the hallmark of Alzheimer’s dementia. Reversely, deposition of Aβ is also responsible for calcium dysregulation. On the other hand, it has been well investigated that viruses can disturb host cell Ca²⁺ homeostasis as well as modulate signal transduction mechanisms. Viruses can also hijack the host cell calcium channels and pumps to release more intracellular Ca²⁺ to utilize for their life cycle. Even though evidence has not been reported on SARS-CoV-2 concerning Ca²⁺ regulation, however, it has been well established that Ca²⁺ is essential for viral entry, viral gene replication, and virion maturation and release. Recent reports suggest that SARS-CoV needs two Ca²⁺ ions to fuse with the host cell at the entry step. Furthermore, some calcium channel blockers (CCBs), such as nimodipine, memantine, etc., have been reported to be effective in the treatment of dementia in Alzheimer’s disease (AD) as well as have shown inhibition in various virus infections.

中文翻译：

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钙通道阻滞剂：治疗SARS-CoV-2感染的阿尔茨海默氏痴呆症患者的潜在治疗策略。

研究表明，钙离子（Ca ²⁺）在阿尔茨海默氏痴呆症和SARS-CoV S介导的融合进入宿主细胞中均起着重要作用。细胞内钙水平升高会引起神经元功能障碍，细胞死亡和细胞凋亡。钙的失调也已显示出增加了淀粉样β（Aβ）蛋白的产生，这是阿尔茨海默氏痴呆症的标志。相反，Aβ的沉积也是钙失调的原因。另一方面，已经充分研究了病毒可以干扰宿主细胞Ca ²⁺稳态以及调节信号转导机制。病毒还可以劫持宿主细胞的钙通道和泵以释放更多的细胞内Ca ²⁺利用他们的生命周期。尽管没有关于SARS-CoV-2的关于Ca ²⁺调节的证据的报道，但是，已经很好地确定了Ca ²⁺对于病毒进入，病毒基因复制以及病毒体成熟和释放至关重要。最近的报告表明，SARS-CoV在进入步骤需要两个Ca ²⁺离子与宿主细胞融合。此外，据报道，某些钙通道阻滞剂（CCBs），例如尼莫地平，美金刚等，可有效治疗阿尔茨海默氏病（AD）中的痴呆症，并已显示出对多种病毒感染的抑制作用。