Instituto de Neurociencias de Alicante, Universidad Miguel Hernández-CSIC, 03550 San Juan de Alicante, Spain.
Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED), 03550 San Juan de Alicante, Spain.
Int J Mol Sci. 2023 Feb 1;24(3):2715. doi: 10.3390/ijms24032715.
The levels of several glial and neuronal plasma biomarkers have been found to increase during the acute phase in COVID-19 patients with neurological symptoms. However, replications in patients with minor or non-neurological symptoms are needed to understand their potential as indicators of CNS injury or vulnerability. Plasma levels of glial fibrillary acidic protein (GFAP), neurofilament light chain protein (NfL), and total Tau (T-tau) were determined by Single molecule array (Simoa) immunoassays in 45 samples from COVID-19 patients in the acute phase of infection [moderate (n = 35), or severe (n = 10)] with minor or non-neurological symptoms; in 26 samples from fully recovered patients after ~2 months of clinical follow-up [moderate (n = 23), or severe (n = 3)]; and in 14 non-infected controls. Plasma levels of the SARS-CoV-2 receptor, angiotensin-converting enzyme 2 (ACE2), were also determined by Western blot. Patients with COVID-19 without substantial neurological symptoms had significantly higher plasma concentrations of GFAP, a marker of astrocytic activation/injury, and of NfL and T-tau, markers of axonal damage and neuronal degeneration, compared with controls. All these biomarkers were correlated in COVID-19 patients at the acute phase. Plasma GFAP, NfL and T-tau levels were all normalized after recovery. Recovery was also observed in the return to normal values of the quotient between the ACE2 fragment and circulating full-length species, following the change noticed in the acute phase of infection. None of these biomarkers displayed differences in plasma samples at the acute phase or recovery when the COVID-19 subjects were sub-grouped according to occurrence of minor symptoms at re-evaluation 3 months after the acute episode (so called post-COVID or "long COVID"), such as asthenia, myalgia/arthralgia, anosmia/ageusia, vision impairment, headache or memory loss. Our study demonstrated altered plasma GFAP, NfL and T-tau levels in COVID-19 patients without substantial neurological manifestation at the acute phase of the disease, providing a suitable indication of CNS vulnerability; but these biomarkers fail to predict the occurrence of delayed minor neurological symptoms.
在伴有神经系统症状的 COVID-19 患者的急性期,已经发现几种神经胶质和神经元的血浆生物标志物的水平升高。然而,需要在有轻微或无神经症状的患者中进行复制,以了解它们作为中枢神经系统损伤或易损性的指标的潜力。通过单分子阵列(Simoa)免疫分析,在 45 例伴有轻微或无神经症状的感染急性期 COVID-19 患者(中度 35 例,重度 10 例)的样本中,测定了神经胶质纤维酸性蛋白(GFAP)、神经丝轻链蛋白(NfL)和总 Tau(T-tau)的血浆水平;在 26 例经过约 2 个月临床随访后完全康复的患者(中度 23 例,重度 3 例)的样本中;以及在 14 例未感染对照者的样本中。还通过 Western blot 测定了 SARS-CoV-2 受体血管紧张素转换酶 2(ACE2)的血浆水平。与对照组相比,无明显神经系统症状的 COVID-19 患者的 GFAP(一种星形胶质细胞激活/损伤的标志物)和 NfL 和 T-tau(轴突损伤和神经元变性的标志物)的血浆浓度显著更高。在 COVID-19 患者的急性期,所有这些生物标志物均相关。康复后,GFAP、NfL 和 T-tau 水平均恢复正常。ACE2 片段与循环全长种之间的比值在感染急性期恢复正常,在恢复过程中也恢复了正常。在感染急性期后 3 个月重新评估时,根据轻微症状(即所谓的后 COVID 或“长 COVID”)的发生将 COVID-19 患者亚组化时,这些标志物在急性期或康复期的血浆样本中均无差异,例如乏力、肌痛/关节痛、嗅觉丧失/味觉丧失、视力障碍、头痛或记忆力减退。我们的研究表明,在疾病的急性期,无明显神经表现的 COVID-19 患者的血浆 GFAP、NfL 和 T-tau 水平发生改变,提示 CNS 易损性;但这些生物标志物不能预测迟发性轻微神经系统症状的发生。