VV and PCG carried out the literature search and created Table1. spread of the computer virus across the globe as well as governmental reactions to the pandemic have had dire effects on human contacts and global economies and instances of panic and depression possess improved in parallel, actually in the non-infected populace [2]. More directly, one study showed that approximately 30% of those infected from the computer virus and who experienced a severe course of the disease also developed mental complaints, such as post-traumatic stress disorder (PTSD) [3]. Another study showed that of 125 severe cases registered as part of the CoroNerve study with neurological and psychiatric presentations of COVID-19 illness, 39 (31%) VCA-2 presented with altered mental status and Flutamide 23 Flutamide (18%) of these fulfilled the medical case meanings for psychiatric disorders including new-onset psychosis, neurocognitive syndrome and affective disorder [4]. Yapici-Eser and colleagues recently explained a potential pathomechanism based on molecular mimicry that may contribute to development of COVID-19-connected neuropsychiatric symptoms [5]. Structural similarities between theN-methyl-d-aspartic acid receptor (NMDAR) GluN1 (synonym NR1) and GluN2a (synonym NR2a) subunits with the SARS-CoV-2 nonstructural protein 8 (NSP8) and 9 (NSP9), respectively, may induce immune-mediated cross-reactivity to the NMDAR. These proteins are essential for replication of the computer virus and may interact directly with glutamate receptors of the NMDA and metabotropic family members, leading to changes in membrane resting-state and action potentials [5]. Molecular mimicry may lead to generation of immunoglobulin G (IgG) antibodies against the NMDAR after SARS-CoV-2 infections. Anti-NMDAR encephalitis, mediated by IgG antibodies to the GluN1 subunit, is definitely a common form of autoimmune encephalitis characterized by demonstration of neurological and psychosis-like symptoms [6]. With this disease, antibodies bind to the NMDAR, induce crosslinking and receptors are consequently internalized and thus are no longer available for excitatory glutamatergic transmission [6]. Viral diseases have been identified as potential causes. For instance, anti-NMDAR-encephalitides can occur as a secondary disease after illness with viruses such as herpes simplex 1 or varicella zoster [7]. Moreover, past influenza A or B infections were identified as Flutamide predisposing factors for NMDAR autoantibody seropositivity [8]. Accordingly, we hypothesized that SARS-CoV-2 might similarly induce anti-NMDAR encephalitis as a direct consequence of illness or secondarily through subsequent activation of autoimmune processes. Viruses such as SARS-CoV-2 hijack the cellular machinery of the sponsor cell in order to reproduce themselves. In the process, their mimicry of key motifs of sponsor proteins can lead to disruption of vital cellular functions, activate swelling pathways and alter the immune response [9]. Here, we aimed to identify published instances of anti-NMDAR encephalitis with concurrent neuropsychiatric symptoms temporally associated with SARS-CoV-2 infections. == Methods == We looked the PubMed and Google Scholar databases using the search terms NMDA encephalitis or NMDAR encephalitis or NMDA receptor encephalitis and SARS-CoV-2 or COVID-19 to identify relevant cases. The last search was performed on September 20th 2021. Preferred Reporting Items for Systematic Evaluations and Meta-Analyses (PRISMA,http://prisma-statement.org) were applied. The process for selecting studies (identification, testing, eligibility and inclusion in the systematic review) is definitely Flutamide reported inside a circulation diagram in Fig.1. Studies were checked for eligibility and selected by two individuals (VV and PCG). In the beginning, many more papers were Flutamide recognized in Google Scholar.