Lithium for COVID-19

Background: Osteoporosis is a progressive bone disease characterized by reduced bone density and deterioration of bone microarchitecture, predominantly affecting the elderly population. The ongoing COVID‐19 pandemic has introduced additional challenges in osteoporosis management, potentially due to systemic inflammation and direct viral impacts on bone metabolism. This study aims to identify common differentially expressed genes (DEGs) and key molecular pathways shared between osteoporosis and COVID‐19, with the goal of uncovering potential therapeutic targets through bioinformatics analysis.Methods: Publicly available gene expression datasets GSE164805 (osteoporosis) and GSE230665 (COVID‐19) were analyzed to identify overlapping DEGs. Functional enrichment analysis using Gene Ontology (GO), pathway analysis, protein–protein interaction (PPI) network construction, and transcription factor (TF)–hub gene regulatory network analysis were performed to explore the biological significance and regulatory mechanisms of these DEGs.Results: A total of 325 common DEGs were identified between osteoporosis and COVID‐19. GO enrichment analysis revealed significant involvement in signal transduction and plasma membrane components. Pathway analysis highlighted the “cytokine–cytokine receptor interaction” pathway as a central player. PPI network analysis identified a module of 193 genes with 397 interactions, from which 10 key hub genes were prioritized: ACTB, CDH1, RPS8, IFNG, RPL17, UBC, RPL36, RPS4Y1, GSK3B, and FGF13. Furthermore, 76 TFs were found to regulate these hub genes, and 15 existing drugs targeting four of these hub genes were identified.Conclusion: This integrative bioinformatics study reveals 15 candidate therapeutic agents that target key regulatory genes shared between osteoporosis and COVID‐19, offering promising treatment strategies for osteoporotic patients, especially those impacted by or at risk of SARS‐CoV‐2​ infection.

Abstract Background Viruses such as Ebola, Marburg, influenza, mpox, MERS-CoV, SARS-CoV, and SARS-CoV-2 pose a significant risk for future pandemics. Developing novel antiviral medicines can be time-consuming and resource intensive. Repurposing existing medicines with antiviral activity offers a faster, cost-effective strategy to expand treatment options during public health emergencies. This scan aimed to identify and synthesise recent evidence on repurposed antiviral medicines under investigation for these viruses. Method A horizon scanning approach was employed, starting with a targeted search in Embase, followed by a systematic search of ClinicalTrials.gov to capture the developmental stages of the technologies. Eligible technologies included UK- or EU-licensed medicines repurposed as antiviral therapies for the viruses of interest. Vaccines, unlicensed medicines, and already approved treatments for the targeted viruses were excluded. Results A total of 196 repurposed technologies targeting the viruses were identified from published literature, and the expanded search on the clinical trials registry yielded 58 technologies in active clinical development. Interventional clinical trial activity was limited to influenza and COVID-19, with 29 technologies for COVID-19 and two for influenza advancing to phase III evaluation. For other viruses, proposed antiviral candidates were identified in the literature but had not progressed into clinical development. Commonly investigated pharmacological classes included direct-acting antivirals, tyrosine kinase inhibitors, immunomodulators, and anti-inflammatory agents. Conclusion Repurposing antiviral medicines represents a pragmatic strategy for rapid therapeutic deployment against emerging viral threats. Collaboration among researchers, policymakers, research funders, and regulatory bodies will be essential to improve pandemic preparedness and support repurposing efforts in emergency situations.

Inositol plays many important roles in cellular processes through its various derivatives including phosphatidylinositol phosphates. Viruses use phosphatidylinositol phosphates for their replication in multiple processes including entry, formation of replication organelles, assembly and release. For these processes, viruses recruit phosphatidylinositol kinases to meet their demand of phosphatidylinositol phosphates. Inhibitors of phosphatidylinositol kinases have been shown to inhibit various viruses. The complexity of various types and isoforms of phosphatidylinositol kinases can be a problem in developing a broad-spectrum antiviral as different viruses use various types and isoforms of the enzyme. Inositol monophosphatase is an enzyme required for both de novo biosynthesis and intracellular recycling of inositol. It can provide a chokepoint to limit the availability of cellular inositol, phosphatidylinositol, and phosphatidylinositol phosphates. It can be a promising target for broad-spectrum antiviral development.

Alpha-synuclein (α-syn) is a 140-amino-acid, intrinsically disordered, soluble protein that is abundantly present in the brain. It plays a crucial role in maintaining cellular structures and organelle functions, particularly in supporting synaptic plasticity and regulating neurotransmitter turnover. However, for reasons not yet fully understood, α-syn can lose its physiological role and begin to aggregate. This altered α-syn disrupts dopaminergic transmission and causes both presynaptic and postsynaptic dysfunction, ultimately leading to cell death. A group of neurodegenerative diseases known as α-synucleinopathies is characterized by the intracellular accumulation of α-syn deposits in specific neuronal and glial cells within certain brain regions. In addition to Parkinson’s disease (PD), these conditions include dementia with Lewy bodies (DLBs), multiple system atrophy (MSA), pure autonomic failure (PAF), and REM sleep behavior disorder (RBD). Given that these disorders are associated with α-syn-related neuroinflammation—and considering that SARS-CoV-2 infection has been shown to affect the nervous system, with COVID-19 patients experiencing neurological symptoms—it has been proposed that COVID-19 may contribute to neurodegeneration in PD and other α-synucleinopathies by promoting α-syn misfolding and aggregation. In this review, we focus on whether SARS-CoV-2 could act as an environmental trigger that facilitates the onset or progression of α-synucleinopathies. Specifically, we present new evidence on the potential role of SARS-CoV-2 in modulating α-syn function and discuss the causal relationship between SARS-CoV-2 infection and the development of parkinsonism-like symptoms.