Diagnostic performance of MRI radiomics for classification of Alzheimer's disease, mild cognitive impairment, and normal subjects: a systematic review and meta-analysis.

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. Radiomics involves extracting quantitative features from medical images and analyzing them using advanced computational algorithms. These characteristics have the potential to serve as biomarkers for disease classification, treatment response prediction, and patient stratification. Of note, 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: 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 August 5, 2023. Original studies discussing the diagnostic performance of MRI radiomics for the classification of AD, MCI, and normal subjects were included. Method quality was evaluated with the Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) and the Radiomics Quality Score (RQS) tools. RESULTS: We identified 13 studies that met the inclusion criteria, involving a total of 5448 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 0.92 (95% CI [0.85; 0.96]) and 0.91 (95% CI [0.85; 0.95]), respectively. The pooled sensitivity and specificity of MRI radiomics for differentiating MCI from normal subjects were 0.74 (95% CI [0.60; 0.85]) and 0.79 (95% CI [0.70; 0.86]), respectively. Also, the pooled sensitivity and specificity of MRI radiomics for differentiating AD from MCI were 0.73 (95% CI [0.64; 0.80]) and 0.79 (95% CI [0.64; 0.90]), 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.

Brain MRI findings in neurologically symptomatic COVID-19 patients: a systematic review and meta-analysis.

BACKGROUND: Coronavirus disease 2019 (COVID-19) has been associated with nervous system involvement, with more than one-third of COVID-19 patients experiencing neurological manifestations. Utilizing a systematic review, this study aims to summarize brain MRI findings in COVID-19 patients presenting with neurological symptoms. METHODS: Systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) checklist. The electronic databases of PubMed/MEDLINE, Embase, Scopus, and Web of Science were systematically searched for literature addressing brain MRI findings in COVID-19 patients with neurological symptoms. RESULTS: 25 publications containing a total number of 3118 COVID-19 patients with neurological symptoms who underwent MRI were included. The most common MRI findings and the respective pooled incidences in decreasing order were acute/subacute infarct (22%), olfactory bulb abnormalities (22%), white matter abnormalities (20%), cerebral microbleeds (17%), grey matter abnormalities (12%), leptomeningeal enhancement (10%), ADEM (Acute Disseminated Encephalomyelitis) or ADEM-like lesions (10%), non-traumatic ICH (10%), cranial neuropathy (8%), cortical gray matter signal changes compatible with encephalitis (8%), basal ganglia abnormalities (5%), PRES (Posterior Reversible Encephalopathy Syndrome) (3%), hypoxic-ischemic lesions (4%), venous thrombosis (2%), and cytotoxic lesions of the corpus callosum (2%). CONCLUSION: The present study revealed that a considerable proportion of patients with COVID-19 might harbor neurological abnormalities detectable by MRI. Among various findings, the most common MRI alterations are acute/subacute infarction, olfactory bulb abnormalities, white matter abnormalities, and cerebral microbleeds.

Partners in crime: Autoantibodies complicit in COVID-19 pathogenesis.

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.

Serum Brain-Derived Neurotrophic Factor (BDNF) in COVID-19 Patients and its Association with the COVID-19 Manifestations.

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.

The role of IL-1 family of cytokines and receptors in pathogenesis of COVID-19.

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.