A global pandemic has erupted as a result of the new brand coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This pandemic has been consociated with widespread mortality worldwide. The antiviral immune response is an imperative factor in confronting the recent coronavirus disease 2019 (COVID-19) infections. Meantime, cytokines recognize as crucial components in guiding the appropriate immune pathways in the restraining and eradication of the virus. Moreover, SARS-CoV-2 can induce uncontrolled inflammatory responses characterized by hyper-inflammatory cytokine production, which causes cytokine storm and acute respiratory distress syndrome (ARDS). As excessive inflammatory responses are contributed to the severe stage of the COVID-19 disease, therefore, the pro-inflammatory cytokines are regarded as the Achilles heel during COVID-19 infection. Among these cytokines, interleukin (IL-) 1 family cytokines (IL-1, IL-18, IL-33, IL-36, IL-37, and IL-38) appear to have a strong inflammatory role in severe COVID-19. Hence, understanding the underlying inflammatory mechanism of these cytokines during infection is critical for reducing the symptoms and severity of the disease. Here, the possible mechanisms and pathways involved in inflammatory immune responses are discussed.

Autoantibodies (AABs) play a critical role in the pathogenesis of autoimmune diseases (AIDs) and serve as a diagnostic and prognostic tool in assessing these complex disorders. Viral infections have long been recognized as a principal environmental factor affecting the production of AABs and the development of autoimmunity. COVID‐19 has primarily been considered a hyperinflammatory syndrome triggered by a cytokine storm. In the following, the role of maladaptive B cell response and AABs became more apparent in COVID‐19 pathogenesis. The current review will primarily focus on the role of extrafollicular B cell response, Toll‐like receptor‐7 (TLR‐7) activation, and neutrophil extracellular traps (NETs) formation in the development of AABs following SARS‐CoV‐2 infection. In the following, this review will clarify how these AABs dysregulate immune response to SARS‐CoV‐2 by disrupting cytokine function and triggering neutrophil hyper‐reactivity. Finally, the pathologic effects of these AABs will be further described in COVID‐19 associate clinical manifestations, including venous and arterial thrombosis, a multisystem inflammatory syndrome in children (MIS‐C), acute respiratory distress syndrome (ARDS), and recently described post‐acute sequelae of COVID‐19 (PASC) or long‐COVID.

COVID-19 is a systematic disease that frequently implies neurological and non-neurological manifestations, predominantly by inducing hypoxia. Brain-derived neurotrophic factor (BDNF) is a key factor in regulating functions of nervous and respiratory systems and has been strongly related to hypoxia. Therefore, this study planned to investigate BDNF association with the COVID-19 manifestations especially neurological impairments and the infection-induced hypoxia. We enrolled sixty-four COVID-19 patients and twenty-four healthy individuals in this study. Patients were divided into two groups, with and without neurological manifestations, and their serum BDNF levels were measured by enzyme-linked immunosorbent assay (ELISA). COVID-19 patients had significantly lower BDNF levels than healthy individuals ( p = 0.023). BDNF levels were significantly lower in patients with neurological manifestations compared to healthy individuals ( p = 0.010). However, we did not observe a statistically significant difference in BDNF levels between patients with and without neurological manifestations ( p = 0.175). BDNF’s levels were significantly lower in patients with CNS manifestations ( p = 0.039) and higher in patients with fever ( p = 0.03) and dyspnea ( p = 0.006). Secondly, BDNF levels have a significant negative association with oxygen therapy requirement ( p = 0.015). These results strongly suggest the critical association between dysregulated BDNF and hypoxia in promoting COVID-19 manifestations, particularly neurological impairments. Supplementary Information The online version contains supplementary material available at 10.1007/s12031-022-02039-1.

Background: Alzheimer's disease (AD) is a debilitating neurodegenerative disease. Early diagnosis of AD and its precursor, mild cognitive impairment (MCI), is crucial for timely intervention and management. Magnetic resonance imaging (MRI) radiomics showed a promising result for diagnosing and classifying AD, and MCI from normal subjects. Thus, we aimed to systematically evaluate the diagnostic performance of the MRI radiomics for this task. Methods and materials: This study was performed using the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) guidelines. A comprehensive search of the current literature was conducted using relevant keywords in PubMed/MEDLINE, Embase, Scopus, and Web of Science databases from inception to October 17, 2022. Original studies discussing the diagnostic performance of MRI Radiomics in Alzheimer's disease (AD), and mild cognitive impairment (MCI) diagnosis were included. Method quality was evaluated with the Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2), and the Radiomic Quality Score tool (RQS). Results: We identified 10 studies that met the inclusion criteria, involving a total of 3446 participants. The overall quality of the included studies was moderate to high. The pooled sensitivity and specificity of MRI radiomics for differentiating AD from normal subjects were 0.8822 (95% CI 0.7888-0.9376), and 0.8849 (95% CI 0.7978-0.9374), respectively. The pooled sensitivity and specificity of MRI radiomics for differentiating MCI from normal subjects were 0.7882 (95% CI 0.6272-0.8917) and 0.7736 (95% CI 0.6480-0.8639), respectively. Also, the pooled sensitivity and specificity of MRI radiomics for differentiating AD from MCI were 0.6938 (95% CI 0.6465-0.7374) and 0.8173 (95% CI 0.6117-0.9270), respectively. Conclusion: MRI radiomics has promising diagnostic performance in differentiating AD, MCI, and normal subjects. It can potentially serve as a non-invasive and reliable tool for early diagnosis and classification of AD and MCI. However, further studies with larger sample sizes and more rigorous study designs are warranted to confirm these findings and establish the clinical utility of MRI radiomics in AD and MCI diagnosis.

Purpose: The coronavirus disease 2019 (COVID-19) is surrounded the world and is associated with multiorgan damage. Olfactory dysfunction is a common manifestation in COVID-19 patients, and in some cases, presents before the coryza signs. We conducted this umbrella review to provide a practical guide on managing, imaging findings, and follow-up of COVID-19 patients with olfactory dysfunction (OD). Methods: A comprehensive search was performed in PubMed, Embase, Scopus, and Web of Science databases from December 2019 until the end of July 2022. Systematic reviews and meta-analyses addressing management and imaging findings of the olfactory manifestations of COVID-19 were included in the study. The quality assessment of included articles was carried out using the Assessment of Multiple Systematic Reviews-2 (AMSTAR-2) tool. Results: A total of 23 systematic reviews were reviewed in this umbrella review. The number of included studies varied between 2 to 155 articles. Several demographic variables were not adequately reported across all the included systematic reviews, including age, gender, preexisting comorbidities, or whether participants had been hospitalized or admitted to the intensive care unit (ICU) due to COVID‐19. Conclusion: It seems that the coronavirus can infect olfactory system structures that play roles in the transmission and interpretation of smell sense. Based on studies, a large proportion of patients experienced OD following COVID-19 infection, and the majority of OD was resolved spontaneously. The possibility of long-lasting OD was higher in young adults with moderate clinical manifestation. Olfactory training (OT) was the most effective therapy. Intranasal corticosteroids (ICS) are also recommended.