Institute for Mind and Biology, Department of Psychology, The University of Chicago, Chicago, Illinois.
J Neurophysiol. 2022 Aug 1;128(2):436-444. doi: 10.1152/jn.00255.2022. Epub 2022 Jul 27.
Olfactory dysfunction is a hallmark symptom of COVID-19 disease resulting from the SARS-CoV-2 virus. The cause of the sudden and usually temporary anosmia that most people suffer from COVID-19 is likely entirely peripheral-inflammation and other damage caused by the virus in the sensory epithelium inside the upper recesses of the nasal cavity can damage or prevent chemicals from properly activating the olfactory sensory neurons. However, persistent olfactory dysfunction from COVID-19, in the form of hyposmia and parosmia (decreased or altered smell) may affect as many as 15 million people worldwide. This epidemic of olfactory dysfunction is thus a continuing public health concern. Mounting evidence suggests that the SARS-CoV-2 virus itself or inflammation from the immune response in the nasal sensory epithelium may invade the olfactory bulb, likely via non-neuronal transmission. COVID-19-related long-term olfactory dysfunction and early damage to olfactory and limbic brain regions suggest a pattern of degeneration similar to that seen in early stages of Alzheimer's disease, Parkinson's disease, and Lewy body dementia. Thus, long-term olfactory dysfunction coupled with cognitive and emotional disturbance from COVID-19 may be the first signs of delayed onset dementia from neurodegeneration. Few treatments are known to be effective to prevent further degeneration, but the first line of defense against degeneration may be olfactory and environmental enrichment. There is a pressing need for more research on treatments for olfactory dysfunction and longitudinal studies including cognitive and olfactory function from patients who have recovered from even mild COVID-19. More than 15 million people worldwide experience persistent COVID-19 olfactory dysfunction, possibly caused by olfactory bulb damage. SARS-CoV-2 can cause inflammation and viral invasion of the olfactory bulb, initiating a cascade of degeneration similar to Alzheimer's disease and Lewy body disease. People who have had even mild cases of COVID-19 show signs of degeneration in cortical areas connected with the olfactory system. These data suggest a wave of post-COVID dementia in the coming decades.
嗅觉功能障碍是 COVID-19 疾病的标志性症状，由 SARS-CoV-2 病毒引起。大多数人患 COVID-19 时所经历的突发性且通常是暂时性嗅觉丧失的原因可能完全是外周性的——病毒在上鼻道的感觉上皮中引起的炎症和其他损伤可破坏或阻止化学物质使嗅觉感觉神经元正常激活。然而，COVID-19 导致的持续性嗅觉功能障碍（表现为嗅觉减退和嗅觉异常，即嗅觉下降或嗅觉改变）可能会影响全球多达 1500 万人。因此，这种嗅觉功能障碍的流行是一个持续存在的公共卫生问题。越来越多的证据表明，SARS-CoV-2 病毒本身或鼻感觉上皮的免疫反应炎症可能会通过非神经元传播侵犯嗅球。COVID-19 相关的长期嗅觉功能障碍以及嗅球和边缘脑区的早期损伤提示存在一种类似于阿尔茨海默病、帕金森病和路易体痴呆早期阶段所见的退化模式。因此，COVID-19 引起的长期嗅觉功能障碍以及认知和情绪障碍可能是神经退行性疾病所致迟发性痴呆的最初迹象。目前已知很少有治疗方法可有效预防进一步退化，但预防退化的第一道防线可能是嗅觉和环境丰富。非常需要开展更多针对嗅觉功能障碍的治疗方法的研究，并对从甚至轻度 COVID-19 中康复的患者进行包括认知和嗅觉功能在内的纵向研究。全球有超过 1500 万人患有持续性 COVID-19 嗅觉功能障碍，可能是嗅球损伤所致。SARS-CoV-2 可引起嗅球炎症和病毒侵袭，引发类似于阿尔茨海默病和路易体病的退化级联反应。即使患有轻度 COVID-19 的患者也显示出与嗅觉系统相关的皮质区域退化的迹象。这些数据提示在未来几十年内会出现一波 COVID-19 后痴呆。
