Background and Aims The coronavirus disease 2019 (COVID‐19), which has caused a global pandemic, is brought on by the Acute Respiratory Syndrome coronavirus 2 (SARS‐CoV‐2). Since the COVID‐19 pandemic started so recently, dealing with complications that emerge years later and have the potential to cause several crises for humanity is one of the issues we face in the post‐COVID‐19 age. Therefore, we wish to discuss a theory and potential dangers surrounding the probability of schizophrenia following COVID‐19 infection in this study. Methods The literature search for this article has been entirely internet‐based. Information was gathered using the Web of Science, PubMed, Scopus, and Google Scholar databases. Results The results showed that multiple immune system changes brought on by COVID‐19 have been identified as potential causes of schizophrenia. Conclusion It is predicted that one of the long‐term effects of COVID‐19 is an increase in the risk of schizophrenia incidence based on the results of this study, which looked at the pathophysiology and etiology of schizophrenia as well as the pathogenic mechanisms of the SARS‐CoV‐2. Therefore, healthcare staff should be prepared to handle any potential risks in future.

The case report describes a post‐COVID‐19 patient with severe right upper quadrant (RUQ) pain, moderate epigastric pain, high troponin levels, and nonspecific ST‐segment and T‐wave changes on electrocardiogram (ECG).

The aim of the present study was to evaluate the effect of rosiglitazone (RSG) or pioglitazone (POG) on the synaptic plasticity, neuronal apoptosis and brain-derived neurotrophic factor (BDNF) and nitric oxide(NO) metabolites in the hippocampus of juvenile hypothyroid rats. The animals were divided into four groups: (1) control, (2) propylthiouracil (PTU), (3) PTU–POG and (4) PTU–RZG. A 0.05% dose of PTU was administered in drinking water for 42 consecutive days. The POG (20 mg/ kg) and the RSG (4 mg/kg) were administered by intraperitoneal (IP) injection on a daily basis. To evaluate synaptic plasticity, we conducted long-term potentiation (LTP) in the Cornuammonist 1 (CA1) area of the hippocampus by high-frequency stimulation of the Schaffer collateral pathway. Then, the hippocampal tissues were collected to determine BDNF and NO levels. In addition, 5 animals from each group also were treated and the brains of animals were collected for apoptosis studies. PTU administration decreased slope, slope 10–90%, and amplitude of fEPSP compared to the control group. Injection of RSG or POG increased the slope, slope 10–90%, and amplitude of fEPSP in the PTU-POG or PTU-RSG groups in comparison to the PTU group. TUNEL positive neurons and NO metabolites in the hippocampus of the PTU group were higher than that of the control. PTU administration attenuated BDNF content, and RSG or POG increased BDNF content in PTU–POG or PTU–RSG groups. Treatment of the rats by POG or RSG decreased apoptotic neurons and NO metabolites in the hippocampus of PTU–POG or PTU–RSG groups compared to the PTU group. The results of this study revealed that POG or RSG normalized LTP impairment, neuronal apoptosis, and improved BDNF content in the hippocampal tissue of juvenile hypothyroid rats.