Is human cytomegalovirus a potential risk factor for mood disorders? A systematic review and meta-analysis.

Mood disorders are among the common mental disorders worldwide. Because of the persistence of cytomegalovirus (CMV) in the body and nervous system, this virus can be activated when the immune system is weakened and continues to exert its destructive effects throughout life. This study aimed to investigate the seroprevalence and association of human cytomegalovirus with mood disorders. Eligible articles were extracted using online international databases Science Direct, Medline, Web of Science, Scopus, and Google Scholar between 2000 and 2023. After quality assessment and specific inclusion and exclusion criteria, a total of eight eligible articles were included in the meta-analysis. Our finding showed that the seropositivity of CMV in mood disorders was 51.6% (95% CI; 42.8-60.4). There were statistical differences between mood disorders and control groups regarding the seropositivity of CMV 1.327% (95% CI; 13.27-10.45). The results of the publication bias using the Egger test confirmed no publication bias in each sub-group. The results of this meta-analysis study demonstrated that CMV infection might have associations with the incidence of mood disorders. Furthermore, we found that there were statistical differences between mood disorders and control groups regarding the seropositivity of CMV.

Role of the cannabinoid CB1 receptor in methamphetamine-induced social and recognition memory impairment.

Methamphetamine (METH) has been reported to induce social and recognition memory impairment. Evidence suggests that the cannabinoid system has an important modulatory role in cognitive processing and social interaction. Nonetheless, no previous study has investigated the probable role of the cannabinoids system on METH-induced deficits of novel object recognition (NOR) memory and social interaction. Adult male rats were given a neurotoxic METH regimen (four injections of 6 mg/kg, s.c, at 2 h intervals). One week later, they were examined for either NOR or social interaction in different groups. The cannabinoid type 1 receptor (CB1R) antagonist rimonabant (1 or 3 mg/kg, i.p.) improved METH-induced impairment of the acquisition, consolidation, and retrieval, but not reconsolidation, of NOR and also METH-induced impairment of social behavior. Administration of the CB1R agonist WIN 55,212-2 (WIN; 3 or 5 mg/kg, i.p.) did not affect memory deficits or social behavior impairment induced by METH. Our findings may indicate that METH neurotoxicity impairs social and recognition memory. On the other hand, the CB1R antagonist rimonabant, but not the CB1R agonist WIN, prevented these negative effects of METH neurotoxicity. Thus, it seems that the CB1R can be targeted to prevent the adverse effects of METH on cognition and social behavior, at least at experimental levels.

Implication of thyroid hormone receptors in methamphetamine neurocognitive effects.

Methamphetamine (MA) induces neurocognitive effects via several mechanisms. In the present study, we investigated the alteration of thyroid hormone receptor's expression in the context of MA-induced memory impairment and explored the protective effects of exogenous thyroid hormones (THs). Male wistar rats, received increasing regimen of MA (1-10 mg/kg, intraperitoneal, twice a day for 10 days), were treated with T3 (40 µg/rat/day; intranasal, 2.5 µl/nostril) or T4 (20 µg/kg/day; intraperitoneal) for 7 days after MA cessation. All rats were subjected to novel object recognition memory test and then the mRNA levels of TH nuclear receptors (TRα1 and TRß1) and seladin-1, an anti-apoptotic factor, and the protein level of TH cell surface receptor (integrin αvß3) were measured in the hippocampus of rats. Our results showed that MA-induced memory impairment is concomitant with decreased level of TRα1 mRNA. T3 or T4 treatment significantly alleviated MA-induced memory impairment, but had no significant effect on the mRNA levels of TH nuclear receptors. However, T4 treatment significantly increased the protein level of cell surface receptor (αv subunit) in MA-treated rats. These findings suggest that MA neurocognitive effects can be associated with impaired TH signaling in the brain and introduce this pathway as a promising therapeutic approach against MA-induced memory impairment.