Effect of alcohol on Brain-Derived Neurotrophic Factor (BDNF) blood levels: a systematic review and meta-analysis.

Brain-Derived Neurotrophic Factor (BDNF) is a vital protein involved in neuronal development, survival, and plasticity. Alcohol consumption has been implicated in various neurocognitive deficits and neurodegenerative disorders. However, the impact of alcohol on BDNF blood levels remains unclear. This systematic review and meta-analysis aimed to investigate the effect of alcohol consumption on BDNF blood levels. A comprehensive search of electronic databases was conducted to identify relevant studies. Eligible studies were selected based on predefined inclusion criteria. Data extraction was performed, and methodological quality was assessed using appropriate tools. A meta-analysis was conducted to estimate the overall effect size of alcohol consumption on BDNF levels. A total of 25 studies met the inclusion criteria and were included in the final analysis. Alcohol use and BDNF blood levels were significantly correlated, according to the meta-analysis (p = 0.008). Overall, it was discovered that drinking alcohol significantly decreased BDNF levels (SMD: - 0.39; 95% CI: - 0.68 to - 0.10; I2: 93%). There was a non-significant trend suggesting that alcohol withdrawal might increase BDNF levels, with an SMD of 0.26 (95% CI: - 0.09 to 0.62; I2: 86%; p = 0.14). Subgroup analysis based on the source of BDNF demonstrated significant differences between the subgroups (p = 0.0008). No significant publication bias was observed. This study showed that alcohol consumption is associated with a significant decrease in BDNF blood levels. The findings suggest a negative impact of alcohol on BDNF levels regardless of alcohol dosage. Further studies are needed to strengthen the evidence and elucidate the underlying mechanisms.

Reactivation of herpesviruses during COVID-19: A systematic review and meta-analysis.

To provide a comprehensive systematic review and meta-analysis regarding the cumulative incidence (incidence proportion) of human herpesvirus (HHV) reactivation among patients with coronavirus disease 2019 (COVID-19), we searched PubMed/MEDLINE, Web of Science, and EMBASE up to 25 September 2022, with no language restrictions. All interventional and observational studies enrolling patients with confirmed COVID-19 and providing data regarding HHV reactivation were included. The random-effects model was used in the meta-analyses. We included information from 32 studies. HHV reactivation was considered a positive polymerase chain reaction result taken at the time of COVID-19 infection. Most of the included patients were severe COVID-19 cases. The pooled cumulative incidence estimate was 38% (95% Confidence Intervals [CI], 28%-50%, I2  = 86%) for herpes simplex virus (HSV), 19% (95% CI, 13%-28%, I2  = 87%) for cytomegalovirus (CMV), 45% (95% CI, 28%-63%, I2  = 96%) for Epstein-Barr virus (EBV), 18% (95% CI, 8%-35%) for human herpesvirus 6 (HHV-6), 44% (95% CI, 32%-56%) for human herpesvirus 7 (HHV-7), and 19% (95% CI, 14%-26%) for human herpesvirus 8 (HHV-8). There was no evidence of funnel plot asymmetry based on visual inspection and Egger's regression test for the results of HSV (p = 0.84), CMV (p = 0.82), and EBV (p = 0.27) reactivation. In conclusion, the identification of HHV reactivation in severe COVID-19 patients is helpful in the management of patients as well as the prevention of complications. Further research is required to elucidate the interaction between HHVs and COVID-19. Systematic review registration: PROSPERO CRD42022321973.