Aging Brain and Cognition Laboratory, Department of Behavioral Science, College of Medicine, University of Kentucky, Lexington, Kentucky, USA.
Sanders Brown Center on Aging, College of Medicine, University of Kentucky, Lexington, Kentucky, USA.
Alzheimers Dement. 2024 Oct;20(10):7296-7319. doi: 10.1002/alz.14089. Epub 2024 Aug 29.
Many coronavirus disease 2019 (COVID-19) positive individuals exhibit abnormal electroencephalographic (EEG) activity reflecting "brain fog" and mild cognitive impairments even months after the acute phase of infection. Resting-state EEG abnormalities include EEG slowing (reduced alpha rhythm; increased slow waves) and epileptiform activity. An expert panel conducted a systematic review to present compelling evidence that cognitive deficits due to COVID-19 and to Alzheimer's disease and related dementia (ADRD) are driven by overlapping pathologies and neurophysiological abnormalities. EEG abnormalities seen in COVID-19 patients resemble those observed in early stages of neurodegenerative diseases, particularly ADRD. It is proposed that similar EEG abnormalities in Long COVID and ADRD are due to parallel neuroinflammation, astrocyte reactivity, hypoxia, and neurovascular injury. These neurophysiological abnormalities underpinning cognitive decline in COVID-19 can be detected by routine EEG exams. Future research will explore the value of EEG monitoring of COVID-19 patients for predicting long-term outcomes and monitoring efficacy of therapeutic interventions. HIGHLIGHTS: Abnormal intrinsic electrophysiological brain activity, such as slowing of EEG, reduced alpha wave, and epileptiform are characteristic findings in COVID-19 patients. EEG abnormalities have the potential as neural biomarkers to identify neurological complications at the early stage of the disease, to assist clinical assessment, and to assess cognitive decline risk in Long COVID patients. Similar slowing of intrinsic brain activity to that of COVID-19 patients is typically seen in patients with mild cognitive impairments, ADRD. Evidence presented supports the idea that cognitive deficits in Long COVID and ADRD are driven by overlapping neurophysiological abnormalities resulting, at least in part, from neuroinflammatory mechanisms and astrocyte reactivity. Identifying common biological mechanisms in Long COVID-19 and ADRD can highlight critical pathologies underlying brain disorders and cognitive decline. It elucidates research questions regarding cognitive EEG and mild cognitive impairment in Long COVID that have not yet been adequately investigated.
许多 2019 年冠状病毒病（COVID-19）阳性个体表现出异常的脑电图（EEG）活动，反映出“脑雾”和轻度认知障碍，甚至在感染急性期后数月也是如此。静息状态下的 EEG 异常包括 EEG 减慢（减少阿尔法节律；增加慢波）和癫痫样活动。一个专家小组进行了系统评价，提出了令人信服的证据，表明 COVID-19 和阿尔茨海默病及相关痴呆症（ADRD）引起的认知缺陷是由重叠的病理学和神经生理学异常引起的。在 COVID-19 患者中观察到的 EEG 异常与在神经退行性疾病的早期阶段观察到的异常相似，特别是 ADRD。据推测，在长期 COVID 和 ADRD 中类似的 EEG 异常是由于平行的神经炎症、星形胶质细胞反应、缺氧和神经血管损伤。COVID-19 中认知能力下降的这些神经生理学异常可以通过常规 EEG 检查来检测。未来的研究将探索 EEG 监测 COVID-19 患者对预测长期结局和监测治疗干预效果的价值。
异常的内在电生理脑活动，如 EEG 减慢、阿尔法波减少和癫痫样波，是 COVID-19 患者的特征性发现。EEG 异常有可能作为神经生物标志物，在疾病的早期识别神经并发症，协助临床评估，并评估长期 COVID 患者的认知衰退风险。与 COVID-19 患者相似的内在脑活动减慢通常见于轻度认知障碍和 ADRD 患者。提出的证据支持这样一种观点，即长期 COVID 和 ADRD 的认知缺陷是由重叠的神经生理学异常驱动的，这些异常至少部分是由神经炎症机制和星形胶质细胞反应引起的。确定长期 COVID-19 和 ADRD 中的共同生物学机制可以突出导致脑障碍和认知衰退的关键病理学。它阐明了在长期 COVID-19 中关于认知 EEG 和轻度认知障碍的研究问题，这些问题尚未得到充分研究。
