Sleep is essential to brain function and mental health. Insomnia and obstructive sleep apnea (OSA) are the two most common sleep disorders, and are major public health concerns. Proton magnetic resonance spectroscopy (1H-MRS) is a non-invasive method of quantifying neurometabolite concentrations. Therefore, 1H-MRS studies on individuals with sleep disorders may enhance our understanding of the pathophysiology of these disorders. In this article, we reviewed 1H-MRS studies in insomnia and OSA that reported changes in neurometabolite concentrations. Previous studies have consistently reported insomnia-related reductions in γ-aminobutyric acid (GABA) levels in the frontal and occipital regions, which suggest that changes in GABA are important to the etiology of insomnia. These results may support the hyperarousal theory that insomnia is associated with increased cognitive and physiological arousal. In addition, the severity of insomnia was associated with low glutamate and glutamine levels. Previous studies of OSA have consistently reported reduced N-acetylaspartate (NAA) levels in the frontal, parietooccipital, and temporal regions. In addition, OSA was associated with increased myo-inositol levels. These results may provide evidence that intermittent hypoxia induced by OSA may result in neuronal damage in the brain, which can be related to neurocognitive dysfunction in patients with OSA. The current review summarizes findings related to neurochemical changes in insomnia and OSA. Future well-designed studies using 1H-MRS have the potential to enhance our understanding of the pathophysiology of sleep disorders including insomnia and OSA.

It is well known that sex hormones are potential modulators of brain functions and women experience dynamic hormonal changes during the menstrual cycle. Previous animal studies have reported that the variations in sex hormones over the menstrual cycle may affect cognitive function, emotion, and behavior by altering structures and functional connectivity of the brain. Considering the prevalence of certain neuropsychiatric disorders such as mood and anxiety disorders is relatively high in women, as compared with men, fluctuations of sex hormones over the menstrual cycle may influence the human brain and potentially underlie sex differences in clinical features of several neuropsychiatric disorders. There is, however, little evidence regarding the exact mechanisms underlying the effects of sex hormones on the human brain. In this review, we focused on studies to examine structural and functional changes over the menstrual cycles in women and aimed to provide an up-to-date overview of neuroimaging studies regarding the effects of sex hormonal fluctuations on the brain and behaviors.

Suicide is a leading cause of death worldwide, especially among adolescents and young adults. Considering this fact, it is imperative that we understand the neural mechanisms underlying suicidal thoughts and behaviors in youth from a neurodevelopmental perspective. In this review, we focused on the magnetic resonance imaging studies that examined the neural correlates of suicidal ideations (SI) or attempts (SA) in youth. We reviewed twenty-three cross-sectional studies reporting the structural and functional alterations in association with SI or SA among adolescents and young adults with various mental disorders. The previous literature suggests that the dorsolateral prefrontal cortex, anterior cingulate cortex, and ventral frontolimbic circuit, may play an important role in the pathophysiology of suicidal behavior in youth through altered top-down control over emotion and impulsivity. Future studies with a longitudinal design and using multimodal imaging techniques may be of help to identify novel therapeutic targets specific for youth with suicidal thoughts and behaviors.

Fear conditioning and extinction, which are adaptive processes to learn and avoid potential threats, have essential roles in the pathophysiology of anxiety disorders. Experimental fear conditioning and extinction have been used to identify the mechanism of fear and anxiety in humans. However, the brain-based mechanisms of fear conditioning and extinction are yet to be established. In the current review, we summarized the results of neuroimaging studies that examined the brain changes—functional activity and structures—regarding fear conditioning or extinction in healthy individuals. The functional activity of the amygdala, insula, anterior cingulate gyrus, ventromedial prefrontal cortex, and hippocampus changed dynamically with both fear conditioning and extinction. This review may provide an up-to-date summary that may broaden our understanding of pathophysiological mechanisms of anxiety disorder. In addition, the brain regions that are involved in the fear conditioning and extinction may be considered as potential treatment targets in the future studies.

It is well known that sex hormones are potential modulators of brain functions and women experience dynamic hormonal changes during the menstrual cycle. Previous animal studies have reported that the variations in sex hormones over the menstrual cycle may affect cognitive function, emotion, and behavior by altering structures and functional connectivity of the brain. Considering the prevalence of certain neuropsychiatric disorders such as mood and anxiety disorders is relatively high in women, as compared with men, fluctuations of sex hormones over the menstrual cycle may influence the human brain and potentially underlie sex differences in clinical features of several neuropsychiatric disorders. There is, however, little evidence regarding the exact mechanisms underlying the effects of sex hormones on the human brain. In this review, we focused on studies to examine structural and functional changes over the menstrual cycles in women and aimed to provide an up-to-date overview of neuroimaging studies regarding the effects of sex hormonal fluctuations on the brain and behaviors.

Sleep is essential to brain function and mental health. Insomnia and obstructive sleep apnea (OSA) are the two most common sleep disorders, and are major public health concerns. Proton magnetic resonance spectroscopy (1H-MRS) is a non-invasive method of quantifying neurometabolite concentrations. Therefore, 1H-MRS studies on individuals with sleep disorders may enhance our understanding of the pathophysiology of these disorders. In this article, we reviewed 1H-MRS studies in insomnia and OSA that reported changes in neurometabolite concentrations. Previous studies have consistently reported insomnia-related reductions in γ-aminobutyric acid (GABA) levels in the frontal and occipital regions, which suggest that changes in GABA are important to the etiology of insomnia. These results may support the hyperarousal theory that insomnia is associated with increased cognitive and physiological arousal. In addition, the severity of insomnia was associated with low glutamate and glutamine levels. Previous studies of OSA have consistently reported reduced N-acetylaspartate (NAA) levels in the frontal, parietooccipital, and temporal regions. In addition, OSA was associated with increased myo-inositol levels. These results may provide evidence that intermittent hypoxia induced by OSA may result in neuronal damage in the brain, which can be related to neurocognitive dysfunction in patients with OSA. The current review summarizes findings related to neurochemical changes in insomnia and OSA. Future well-designed studies using 1H-MRS have the potential to enhance our understanding of the pathophysiology of sleep disorders including insomnia and OSA.

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.

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.

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.

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.