Deciphering the Link: Correlating REM Sleep Patterns with Depressive Symptoms via Consumer Wearable Technology.

This study investigates the correlation between REM sleep patterns, as measured by the Apple Watch, and depressive symptoms in an undiagnosed population. Employing the Apple Watch for data collection, REM sleep duration and frequency were monitored over a specified period. Concurrently, participants' depressive symptoms were evaluated using standardized questionnaires. The analysis, primarily using Spearman's correlation, revealed noteworthy findings. A significant correlation was observed between an increased REM sleep proportion and higher depressive symptom scores, with a correlation coefficient of 0.702, suggesting a robust relationship. These results highlight the potential of using wearable technology, such as the Apple Watch, in early detection and intervention for depressive symptoms, suggesting that alterations in REM sleep could serve as preliminary indicators of depressive tendencies. This approach offers a non-invasive and accessible means to monitor and potentially preempt the progression of depressive disorders. This study's implications extend to the broader context of mental health, emphasizing the importance of sleep assessment in routine health evaluations, particularly for individuals exhibiting early signs of depressive symptoms.

The association between the CCDC88A gene polymorphism at rs1437396 and alcohol use disorder, with or without major depression disorder.

Girdin is a protein involved in neuronal migration and hippocampal development. It is encoded by the coiled-coil domain-containing 88A (CCDC88A) gene, located on the short arm of chromosome 2 (2p). The CCDC88A gene is modulated by the intergenic single-nucleotide polymorphism (SNP) of the rs1437396, situated 9.5 kb downstream from its transcription stop site. As recent genome-wide research has associated the T allele of the SNP with increased risk of alcohol use disorder (AUD), we wanted to validate this finding in an independent cohort and to test further for an association with comorbid major depressive disorder (MDD). The study included 226 AUD patients (AUD group), 53 patients with comorbid MDD, and 391 controls selected randomly. The participants were genotyped for the rs1437396 polymorphism using the real-time polymerase chain reaction. The association between the rs1437396 polymorphism and increased risk of AUD and AUD+MDD was tested with logistic regression. Our results show significantly higher frequency of the T risk allele in the AUD group (p=0.027) and even higher in the AUD+MDD group (p=0.016). In conclusion, this is the first study that has validated the association between the rs1437396 polymorphism of the CCDC88A gene and AUD with or without MDD. Studies on larger samples of patients are needed to further investigate the mechanism of this association.

The Modulatory Effect of Metformin on Ethanol-Induced Anxiety, Redox Imbalance, and Extracellular Matrix Levels in the Brains of Wistar Rats.

The study investigated the potential neuroprotective effects of metformin (MET) on alcohol-induced neurotoxicity in adult Wistar rats. The animals were randomized in four groups (n = 10): control, alcohol (ALC), ALC + MET, and MET. ALC (2 g/kg b.w.) and MET (200 mg/kg b.w.) were orally administered for 21 days, once daily. For the ALC + MET group, MET was administered 2 h after ALC treatment. On day 22, the open field test (OFT) and elevated plus maze (EPM) were performed. MET improved global activity and increased the time spent in unprotected open arms, decreased oxidative stress, both in the frontal lobe and in the hippocampus, and increased neuroglobin expression in the frontal cortex. Histopathologically, an increased neurosecretory activity in the frontal cortex in the ALC + MET group was noticed. Thus, our findings suggest that metformin has antioxidant and anxiolytic effects and may partially reverse the neurotoxic effects induced by ethanol.