Objectives: Smoking causes 8 million deaths annually and significant socioeconomic burdens. Despite several therapies, cessation rates remain low due to nicotine’s addictive properties and withdrawal symptoms. This study evaluates the efficacy of transcutaneous auricular vagus nerve stimulation (taVNS) in reducing nicotine dependence and improving psychological states. Methods: This pilot study enrolled 23 adult smokers aged 19 to 65 years with the Fagerström Test for Nicotine Dependence (FTND) scores over 4 and daily cigarette consumption exceeding 10. Participants were randomized into treatment and control groups. The treatment group received personalized taVNS stimulation targeting the auricular branch of the vagus nerve, applied for 30 minutes, three times daily, for four weeks. The control group received a low-level fixed-current stimulation. Outcomes, including the FTND, cigarettes per day (CPD), the Patient Health Questionnaire-9 (PHQ-9), the Generalized Anxiety Disorder-7 (GAD-7), and the Insomnia Severity Index (ISI), were assessed at baseline, 2 weeks, and 4 weeks. Statistical analyses included the Mann–Whitney U-test and Wilcoxon signed-rank test. Results: The treatment group showed significant reductions in the FTND (2.0 points at 2 weeks, p<0.05; 3.0 points at 4 weeks, p<0.05) and CPD (1.0 fewer cigarette at 2 weeks, p<0.05; 2.0 fewer cigarettes at 4 weeks, p<0.05). Additionally, the PHQ-9 scores decreased significantly in the treatment group (3.0 points at 2 weeks, p<0.05; no further improvement at 4 weeks). However, the GAD-7 and the ISI scores showed no statistically significant changes in either group. The control group exhibited slight improvements in the FTND and the CPD, possibly due to placebo effects or motivation induced by study participation. Conclusions This study highlights taVNS as a promising non-invasive treatment for smoking cessation, effective in reducing nicotine dependence and improving depressive symptoms. However, its effects on anxiety and sleep quality remain unclear. Larger studies are needed to confirm its efficacy and explore optimal parameters and underlying mechanisms.

Late life depression (LLD) is common and characterized by specific cognitive decline, numerous comorbidies accompanied by consideration of polypharmacy, and heavy disability. Distinct structural and functional changes observed in neuroimaging lead to neurobehavioral symptoms in this population. Dysfunction of the default mode network, cognitive control network, anterior salience network, and positive valence system circuits brings about negative self-referential rumination, executive function problem, troubles in attention, and reward processing deficit. Due to frequent cognitive impairment in LLD and strong association between Alzheimer’s dementia (AD) and depressive symptoms, discrete elaboration is difficult. There are various linkages between LLD and AD in pathophysiologies including neuroinflammation, vascular disease, and neurodegeneration. These etiological hypotheses are supported by clinical manifestations, cognitive measurements, neuroimage and related molecular findings. Therefore, LLD is thought to be a risk factor for AD which should be managed. However, other perspectives on LLD suggest it as a prodromal manifestation of AD or as prognostic factor to predict disease progression. Consistent research with eligible criteria with homogenous diagnosis, cognitive and symptom measurement, and long-term follow-up studies would be needed to better understand the relationship between LLD and AD.

Objectives: Smoking causes 8 million deaths annually and significant socioeconomic burdens. Despite several therapies, cessation rates remain low due to nicotine’s addictive properties and withdrawal symptoms. This study evaluates the efficacy of transcutaneous auricular vagus nerve stimulation (taVNS) in reducing nicotine dependence and improving psychological states. Methods: This pilot study enrolled 23 adult smokers aged 19 to 65 years with the Fagerström Test for Nicotine Dependence (FTND) scores over 4 and daily cigarette consumption exceeding 10. Participants were randomized into treatment and control groups. The treatment group received personalized taVNS stimulation targeting the auricular branch of the vagus nerve, applied for 30 minutes, three times daily, for four weeks. The control group received a low-level fixed-current stimulation. Outcomes, including the FTND, cigarettes per day (CPD), the Patient Health Questionnaire-9 (PHQ-9), the Generalized Anxiety Disorder-7 (GAD-7), and the Insomnia Severity Index (ISI), were assessed at baseline, 2 weeks, and 4 weeks. Statistical analyses included the Mann–Whitney U-test and Wilcoxon signed-rank test. Results: The treatment group showed significant reductions in the FTND (2.0 points at 2 weeks, p<0.05; 3.0 points at 4 weeks, p<0.05) and CPD (1.0 fewer cigarette at 2 weeks, p<0.05; 2.0 fewer cigarettes at 4 weeks, p<0.05). Additionally, the PHQ-9 scores decreased significantly in the treatment group (3.0 points at 2 weeks, p<0.05; no further improvement at 4 weeks). However, the GAD-7 and the ISI scores showed no statistically significant changes in either group. The control group exhibited slight improvements in the FTND and the CPD, possibly due to placebo effects or motivation induced by study participation. Conclusions This study highlights taVNS as a promising non-invasive treatment for smoking cessation, effective in reducing nicotine dependence and improving depressive symptoms. However, its effects on anxiety and sleep quality remain unclear. Larger studies are needed to confirm its efficacy and explore optimal parameters and underlying mechanisms.

Late life depression (LLD) is common and characterized by specific cognitive decline, numerous comorbidies accompanied by consideration of polypharmacy, and heavy disability. Distinct structural and functional changes observed in neuroimaging lead to neurobehavioral symptoms in this population. Dysfunction of the default mode network, cognitive control network, anterior salience network, and positive valence system circuits brings about negative self-referential rumination, executive function problem, troubles in attention, and reward processing deficit. Due to frequent cognitive impairment in LLD and strong association between Alzheimer’s dementia (AD) and depressive symptoms, discrete elaboration is difficult. There are various linkages between LLD and AD in pathophysiologies including neuroinflammation, vascular disease, and neurodegeneration. These etiological hypotheses are supported by clinical manifestations, cognitive measurements, neuroimage and related molecular findings. Therefore, LLD is thought to be a risk factor for AD which should be managed. However, other perspectives on LLD suggest it as a prodromal manifestation of AD or as prognostic factor to predict disease progression. Consistent research with eligible criteria with homogenous diagnosis, cognitive and symptom measurement, and long-term follow-up studies would be needed to better understand the relationship between LLD and AD.

Objectives: Smoking causes 8 million deaths annually and significant socioeconomic burdens. Despite several therapies, cessation rates remain low due to nicotine’s addictive properties and withdrawal symptoms. This study evaluates the efficacy of transcutaneous auricular vagus nerve stimulation (taVNS) in reducing nicotine dependence and improving psychological states. Methods: This pilot study enrolled 23 adult smokers aged 19 to 65 years with the Fagerström Test for Nicotine Dependence (FTND) scores over 4 and daily cigarette consumption exceeding 10. Participants were randomized into treatment and control groups. The treatment group received personalized taVNS stimulation targeting the auricular branch of the vagus nerve, applied for 30 minutes, three times daily, for four weeks. The control group received a low-level fixed-current stimulation. Outcomes, including the FTND, cigarettes per day (CPD), the Patient Health Questionnaire-9 (PHQ-9), the Generalized Anxiety Disorder-7 (GAD-7), and the Insomnia Severity Index (ISI), were assessed at baseline, 2 weeks, and 4 weeks. Statistical analyses included the Mann–Whitney U-test and Wilcoxon signed-rank test. Results: The treatment group showed significant reductions in the FTND (2.0 points at 2 weeks, p<0.05; 3.0 points at 4 weeks, p<0.05) and CPD (1.0 fewer cigarette at 2 weeks, p<0.05; 2.0 fewer cigarettes at 4 weeks, p<0.05). Additionally, the PHQ-9 scores decreased significantly in the treatment group (3.0 points at 2 weeks, p<0.05; no further improvement at 4 weeks). However, the GAD-7 and the ISI scores showed no statistically significant changes in either group. The control group exhibited slight improvements in the FTND and the CPD, possibly due to placebo effects or motivation induced by study participation. Conclusions This study highlights taVNS as a promising non-invasive treatment for smoking cessation, effective in reducing nicotine dependence and improving depressive symptoms. However, its effects on anxiety and sleep quality remain unclear. Larger studies are needed to confirm its efficacy and explore optimal parameters and underlying mechanisms.

Late life depression (LLD) is common and characterized by specific cognitive decline, numerous comorbidies accompanied by consideration of polypharmacy, and heavy disability. Distinct structural and functional changes observed in neuroimaging lead to neurobehavioral symptoms in this population. Dysfunction of the default mode network, cognitive control network, anterior salience network, and positive valence system circuits brings about negative self-referential rumination, executive function problem, troubles in attention, and reward processing deficit. Due to frequent cognitive impairment in LLD and strong association between Alzheimer’s dementia (AD) and depressive symptoms, discrete elaboration is difficult. There are various linkages between LLD and AD in pathophysiologies including neuroinflammation, vascular disease, and neurodegeneration. These etiological hypotheses are supported by clinical manifestations, cognitive measurements, neuroimage and related molecular findings. Therefore, LLD is thought to be a risk factor for AD which should be managed. However, other perspectives on LLD suggest it as a prodromal manifestation of AD or as prognostic factor to predict disease progression. Consistent research with eligible criteria with homogenous diagnosis, cognitive and symptom measurement, and long-term follow-up studies would be needed to better understand the relationship between LLD and AD.

Objectives: Smoking causes 8 million deaths annually and significant socioeconomic burdens. Despite several therapies, cessation rates remain low due to nicotine’s addictive properties and withdrawal symptoms. This study evaluates the efficacy of transcutaneous auricular vagus nerve stimulation (taVNS) in reducing nicotine dependence and improving psychological states. Methods: This pilot study enrolled 23 adult smokers aged 19 to 65 years with the Fagerström Test for Nicotine Dependence (FTND) scores over 4 and daily cigarette consumption exceeding 10. Participants were randomized into treatment and control groups. The treatment group received personalized taVNS stimulation targeting the auricular branch of the vagus nerve, applied for 30 minutes, three times daily, for four weeks. The control group received a low-level fixed-current stimulation. Outcomes, including the FTND, cigarettes per day (CPD), the Patient Health Questionnaire-9 (PHQ-9), the Generalized Anxiety Disorder-7 (GAD-7), and the Insomnia Severity Index (ISI), were assessed at baseline, 2 weeks, and 4 weeks. Statistical analyses included the Mann–Whitney U-test and Wilcoxon signed-rank test. Results: The treatment group showed significant reductions in the FTND (2.0 points at 2 weeks, p<0.05; 3.0 points at 4 weeks, p<0.05) and CPD (1.0 fewer cigarette at 2 weeks, p<0.05; 2.0 fewer cigarettes at 4 weeks, p<0.05). Additionally, the PHQ-9 scores decreased significantly in the treatment group (3.0 points at 2 weeks, p<0.05; no further improvement at 4 weeks). However, the GAD-7 and the ISI scores showed no statistically significant changes in either group. The control group exhibited slight improvements in the FTND and the CPD, possibly due to placebo effects or motivation induced by study participation. Conclusions This study highlights taVNS as a promising non-invasive treatment for smoking cessation, effective in reducing nicotine dependence and improving depressive symptoms. However, its effects on anxiety and sleep quality remain unclear. Larger studies are needed to confirm its efficacy and explore optimal parameters and underlying mechanisms.

Late life depression (LLD) is common and characterized by specific cognitive decline, numerous comorbidies accompanied by consideration of polypharmacy, and heavy disability. Distinct structural and functional changes observed in neuroimaging lead to neurobehavioral symptoms in this population. Dysfunction of the default mode network, cognitive control network, anterior salience network, and positive valence system circuits brings about negative self-referential rumination, executive function problem, troubles in attention, and reward processing deficit. Due to frequent cognitive impairment in LLD and strong association between Alzheimer’s dementia (AD) and depressive symptoms, discrete elaboration is difficult. There are various linkages between LLD and AD in pathophysiologies including neuroinflammation, vascular disease, and neurodegeneration. These etiological hypotheses are supported by clinical manifestations, cognitive measurements, neuroimage and related molecular findings. Therefore, LLD is thought to be a risk factor for AD which should be managed. However, other perspectives on LLD suggest it as a prodromal manifestation of AD or as prognostic factor to predict disease progression. Consistent research with eligible criteria with homogenous diagnosis, cognitive and symptom measurement, and long-term follow-up studies would be needed to better understand the relationship between LLD and AD.

Mood disorders are a major cause of morbidity. Many patients experience treatment-resistant depression, and suicide rates are on the rise. There is a critical need for faster-acting and more effective antidepressants. After decades of research, esketamine, initially used as an anesthetic, has begun to be used as an outpatient treatment for major depressive disorder. Esketamine, an N-methyl-D-aspartate receptor antagonist, directly targets the glutamate system, rapidly improving mood symptoms and reducing suicidal ideation. Esketamine has demonstrated superior efficacy in reducing depressive symptoms more quickly than traditional oral antidepressant monotherapy, with a favorable risk-benefit profile. Reported side effects include sedation, dizziness, dissociative reactions, and increased blood pressure, though these effects are generally limited to the monitoring period of approximately two hours following administration.

Objectives: Recent advances in brain age prediction models reveal accelerated brain aging in major depressive disorder (MDD) patients. This review investigates the complex relationship between brain aging and biological age gap (BAG) in MDD, emphasizing the influences of clinical characteristics, treatment responses, and various neuroimaging techniques on this dynamic interplay. Methods: A systematic review of the existing literature was conducted, focusing on 18 studies that analyze brain aging patterns in MDD patients. Key factors such as age, clinical features, and lifestyle choices were examined to assess their impact on BAG and the overall neurobiological health of individuals with MDD. Results: The findings indicate that MDD patients frequently experience accelerated brain aging, particularly in elderly populations, with BAG serving as a valuable biomarker for assessing biological aging rates. The review highlights the urgent need for more granular approaches, considering variables such as age, gender, and socioeconomic status. Specific local brain aging patterns were observed in regions related to emotional regulation, suggesting that localized BAG changes may provide critical insights into the pathophysiology of MDD and its neurobiological underpinnings. Conclusions BAG is a significant biomarker for evaluating accelerated brain aging in MDD, informing personalized treatment strategies. Future research should incorporate diverse clinical characteristics and advanced neuroimaging techniques in representative samples to enhance the clinical applicability of BAG and deepen the understanding of its role in depression and biological aging.