Stress and gender differences in brain development.

A systematic literature review of sex differences in childhood language and brain development

Unprecedented 4D spatiotemporal infant regional cerebral blood flow framework and region-specific physiology–function coupling across infancy were elucidated, highlighting strong physiology–function coupling specifically at the default-mode network to meet extraneuronal metabolic demand for network emergence.

Maternal Depression and Child Development: Clues to Causal Mechanisms From Potential Confounders.

INTRODUCTION:Various chronic pain conditions go along with functional and structural brain changes. This study aimed to investigate functional and structural brain changes by magnetic resonance imaging (MRI) in inflammatory bowel disease (IBD) patients with chronic abdominal pain.METHODS:Sixty-four subjects were included in the final analysis (32 IBD patients with chronic abdominal pain; 32 age-matched and sex-matched controls). All patients suffered from chronic abdominal pain, defined as a score of ≥3/10 on the visual analog scale for at least 3 months in the past 6 months. Besides structural MRI, resting state functional MRI was used to compare functional connectivity of 10 networks between groups.RESULTS:Patients with IBD showed no structural brain alterations but a significantly increased resting state functional connectivity of the secondary somatosensory cortex within the salience network.DISCUSSION:Because the secondary somatosensory cortex saves sensory stimuli and compares novel information with latter experiences, these functions may be maladaptive in IBD patients with abdominal pain.

Introduction: Sleep disorders (SLD) are supposed to be associated with increased risk and development of Alzheimer's disease (AD), and patients with AD are more likely to show SLD. However, neurobiological performance of patients with both AD and SLD in previous studies is inconsistent, and identifying specific patterns of the brain functional network and structural characteristics in this kind of comorbidity is warranted for understanding how AD and SLD symptoms interact with each other as well as finding effective clinical intervention. Thus, the aims of this systematic review were to summarize the relevant findings and their limitations and provide future research directions.Methods: A systematic search on brain functional and structural changes in patients with both AD and SLD was conducted from PubMed, Web of Science, and EMBASE databases.Results: Nine original articles published between 2009 and 2021 were included with a total of 328 patients with comorbid AD and SLD, 367 patients with only AD, and 294 healthy controls. One single-photon emission computed tomography study and one multislice spiral computed tomography perfusion imaging study investigated changes of cerebral blood flow; four structural magnetic resonance imaging (MRI) studies investigated brain structural changes, two of them used whole brain analysis, and another two used regions of interest; two resting-state functional MRI studies investigated brain functional changes, and one 2-deoxy-2-(18F)fluoro-d-glucose positron emission tomography (18F-FDG-PET) investigated 18F-FDG-PET uptake in patients with comorbid AD and SLD. Findings were inconsistent, ranging from default mode network to sensorimotor cortex, hippocampus, brain stem, and pineal gland, which may be due to different imaging techniques, measurements of sleep disorder and subtypes of AD and SLD.Conclusions: Our review provides a systematic summary and promising implication of specific neuroimaging dysfunction underlying co-occurrence of AD and SLD. However, limited and inconsistent findings still restrict its neurobiological explanation. Further studies should use unified standards and comprehensive brain indices to investigate the pathophysiological basis of interaction between AD and SLD symptoms in the development of the disease spectrums.

This study aimed to evaluate the neuropsychiatric symptoms of quarantined COVID-19 survivors 15months after discharge and explore its potential association with structural and functional brain changes and inflammation. A total of 51 quarantined COVID-19 survivors and 74 healthy controls were included in this study. Cognitive function was assessed using the THINC-integrated tool. Structural brain changes were examined through both surface- and volume-based analyses, and functional changes were assessed using resting-state amplitude low-frequency fluctuation (ALFF). Serum inflammatory markers were measured by a multiplexed flow cytometric assay. COVID-19 survivors exhibited subjective cognitive decline compared to healthy controls, despite no significant differences in objective cognitive tasks. Structural analysis revealed significantly increased gray matter volume and cortical surface area in the left transverse temporal gyrus (Heschl's gyrus) in quarantined COVID-19 survivors. This enlargement was negatively correlated with cognitive impairment. The ALFF analysis showed decreased neural activity in multiple brain regions. Elevated levels of serum inflammatory markers were also found in COVID-19 survivors, including MIP-1a, MIP-1b, TNF-a, and IL-8, which correlated with functional abnormalities. Our findings indicate a subjective cognitive decline in quarantined COVID-19 survivors 15months after discharge, which is associated with brain structural alterations in the left Heschl's gyrus. The observed elevation of inflammatory markers suggests a potential mechanism involving inflammation-induced neurogenesis. These results contribute to our understanding of the possible mechanisms underlying long-term neuropsychiatric consequences of COVID-19 and highlight the need for further research to develop targeted interventions.

It is commonly believed that alertness and attention decrease after sleep deprivation (SD). However, there are not enough studies on the changes in psychomotor vigilance testing (PVT) during SD and the corresponding changes in brain function and brain structure after SD. Therefore, we recruited 30 healthy adult men to perform a 36 h acute SD experiment, including the measurement of five indicators of PVT every 2 h, and analysis of cerebral blood flow (CBF) and grey matter volume (GMV) changes, before and after SD by magnetic resonance imaging (MRI). The PVT measurement found that the mean reaction time (RT), fastest 10% RT, minor lapses, and false starts all increased progressively within 20 h of SD, except for major lapses. Subsequently, all indexes showed a significant lengthening or increasing trend, and the peak value was in the range of 24 h-32 h and decreased at 36 h, in which the number of major lapses returned to normal. MRI showed that CBF decreased in the left orbital part of the superior frontal gyrus, the left of the rolandic operculum, the left triangular part, and the right opercular part of the inferior frontal gyrus, and CBF increased in the left lingual gyrus and the right superior gyrus after 36 h SD. The left lingual gyrus was negatively correlated with the major lapses, and both the inferior frontal gyrus and the superior frontal gyrus were positively correlated with the false starts. Still, there was no significant change in GMV. Therefore, we believe that 36 h of acute SD causes alterations in brain function and reduces alert attention, whereas short-term acute SD does not cause changes in brain structure.

Brain structural and functional alterations in individuals with combined overweight/obesity and mood disorders: A systematic review of neuroimaging studies

Intracranial space-occupying lesions (ISOLs) are common pediatric conditions. Recent therapeutic advances have significantly improved survival rates, necessitating increased attention to post-operative cognitive outcomes, which are crucial determinants of patients' quality of life. While previous studies have predominantly focused on short-term post-operative changes, this study aimed to investigate longitudinal changes in cognition, brain structure, and function of the contralateral hemisphere following pediatric neurosurgery. Nineteen pediatric patients with ISOLs were enrolled in a paired design study. Cognitive assessments, structural imaging, and functional imaging data were collected at three time points: pre-operation, first post-operative follow-up (mean 75 days pre-operation), and second post-operative follow-up (mean 316 days pre-operation). Relevant metrics were computed and compared across time points. The majority of cognitive domains exhibited a gradual longitudinal improvement trajectory, with three domains showing significant enhancement at the second follow-up compared to preoperative baseline: cognitive flexibility (t = 4.201, p = 0.001), executive function (t = 3.478, p = 0.003), and social accuracy (t = 3.248, p = 0.004). The contralesional hemisphere demonstrated alterations primarily characterized by gray matter density reduction, progressing from subcortical structures (first follow-up: thalamus, peak intensity = -7.54, cluster p < 0.016) to cortical regions (second follow-up compared to previous follow-up: superior frontal gyrus, peak intensity = -7.80, cluster p < 0.016), followed by a subsequent increase in brain activity power of smaller magnitude (second follow-up: medial superior frontal gyrus, amplitude of low frequency fluctuation, peak intensity = 5.96, cluster p < 0.016). Correlation analysis suggests that there is an association between changes in brain structure and alterations in cognitive function (r = -0.53, p = 0.019). Our findings suggest that post-craniotomy structural and functional brain changes in children follow a subcortical-to-cortical trajectory, with structural alterations (decreased gray matter density) preceding functional activation. This process demonstrates progressive and cumulative characteristics. These modifications appear to correlate with cognitive function recovery and may represent potential mechanisms underlying spontaneous cognitive rehabilitation in pediatric patients post-surgery. Cautiously interpreted, the deeper neuroplastic mechanisms underlying these changes might involve synaptic pruning-like processes induced by external perturbation.

Neuroimaging studies described brain structural changes that comprise the mechanisms underlying individual differences in migraine development and maintenance. However, whether such interindividual variability in migraine was observed in a pretreatment scan is a predisposition for subsequent hypoalgesia to placebo treatment that remains largely unclear. Using T1-weighted imaging, we investigated this issue in 50 healthy controls (HC) and 196 patients with migraine without aura (MO). An 8-week double-blinded, randomized, placebo-controlled acupuncture was used, and we only focused on the data from the sham acupuncture group. Eighty patients participated in an 8-weeks sham acupuncture treatment, and were subdivided (50% change in migraine days from baseline) into recovering (MOr) and persisting (MOp) patients. Optimized voxel-based morphometry (VBM) and functional connectivity analysis were performed to evaluate brain structural and functional changes. At baseline, MOp and MOr had similar migraine activity, anxiety and depression; reduced migraine days were accompanied by decreased anxiety in MOr. In our findings, the MOr group showed a smaller volume in the left medial prefrontal cortex (mPFC), and decreased mPFC-related functional connectivity was found in the default mode network. Additionally, the reduction in migraine days after placebo treatment was significantly associated with the baseline gray matter volume of the mPFC which could also predict post-treatment groups with high accuracy. It indicated that individual differences for the brain structure in the pain modulatory system at baseline served as a substrate on how an individual facilitated or diminished hypoalgesia responses to placebo treatment in migraineurs. Hum Brain Mapp 38:4386-4397, 2017. © 2017 Wiley Periodicals, Inc.

Differences in the development of the male and female brain are an evolving area of investigation. We are beginning to understand the underpinnings of male and female advantages due to differences in brain development as well as the consequences following hypoxic-ischemic brain injury in the newborn. The two main factors that appear to affect outcomes are gestation age at the time of injury and sex of the subject. This review starts with a summary of differences in the anatomy and physiology of the developing male and female brain. This is followed by a review of the major factors responsible for the observed differences in the face of normal development and hypoxic injury. The last section reviews the response of male and female subjects to various neuroprotective strategies that are currently being used and where there is a need for additional information for more precise therapy based on the sex of the infant.

Reviewed by: Reinventing the Sexes: The Biomedical Construction of Femininity and Masculinity Thomas W. Laqueur Marianne van den Wijngaard. Reinventing the Sexes: The Biomedical Construction of Femininity and Masculinity. Race, Gender, and Science series. Bloomington: Indiana University Press, 1997. x + 171 pp. Ill. $29.95 (cloth), $12.95 (paperbound). Enormous scholarly energy in the humanities and social sciences, and a wide range of political and broadly cultural energies as well, have been expended over the past three decades in an effort to disengage gender (behavior that is characterized as masculine or feminine) from sex (the biological foundation of male and female that is supposedly timeless and objective), and to disrupt the very idea of “normality” in the arena of sexuality. Sex, the argument goes, does not dictate gender, nor is it a normative, dimorphic characteristic that needs to be corrected in so-called intersexuals so that a particular genital configuration lines up perfectly with socially prescribed masculine or feminine behavior. These behaviors are not, of course, independent of biology—we exist, after all, in our bodies—but nor are they deeply embedded in it. In this beautifully detailed account, a Dutch biologist and feminist, equally adept at cultural studies of science and developmental endocrinology, first documents the scientific passion for studying sexual difference in general: about 130 articles per year in 1967, and more than 500 in 1984. She then explains how, beginning in 1959, organization theory—the study of how hormones cause the embryonic unisex brain to differentiate into a male or female brain, which in turn accounts for masculine or feminine behavior in the mature animal or human—swept the field and has maintained its hegemony until the present despite the challenges of feminism, a new generation of women researchers, and the publication of a considerable body of critical evidence. Articles on sex differences in brain development, the product of the research program based on the new paradigm, multiplied even faster during the same period: from eight per year to almost a hundred. The triumph of organization theory is extraordinary: hormones had not been expected to play a prenatal role in organizing how an individual responds to the world. Its success, in Wijngaard’s view, depended less on experimental triumphs than on various aspects of the sociology of the relevant sciences and their history: the new paradigm provided a theoretical basis for workers who had begun experimenting on the behavioral effects of hormones; it unified psychological and neurological research and afforded psychologists the prestige of the biomedical [End Page 546] sciences; it appropriated the older assumption of reproductive endocrinology that there were distinct male and female gonadal hormones—androgens and estrogens—which were the determinants of maleness and femaleness more generally; and it served as ammunition in the culture wars raging outside the laboratory around the old nature/nurture debate about sexual biology and social behavior. Women in the laboratory changed the terms of organization theory but did not shake its fundamental assumption: the fixing of sex in the embryonic brain. No longer was the question simply how the embryonic male secreted androgens so as to masculinize his otherwise undifferentiated brain—a dualistic model—but rather how male and female hormones affected behavior in both sexes. But still, work that tended to blur dimorphic distinctions—research, for example, on the very different and distinct effects of estrogen and progestins, both female hormones, in producing behavior that could be characterized as either masculine or feminine—was discounted. Wijngaard argues, in what is perhaps the most original part of the book, that the tenacity of the organization theory model is not due to the failure of feminist criticism of its methodology or fundamental assumptions, nor to the absence of negative evidence, but to its institutional embeddedness. Networks of knowledge are its bulwark: physicians who run clinics that sort out aberrant biology and behavior, journalists who thrive on reports that still another biological marker of difference has been found, scientists sitting on peer review panels whose own research programs are predicated on a dualism firmly etched in the developing brain. The social demands and images of masculinity and femininity thus affect the cognitive development of science via practitioners with an interest...

Addiction is a chronic disease that has serious consequences, both in terms of public health and economy. Clear characteristics distinguish recreational and controlled use from addiction. Thus, today, addiction includes the notions of compulsive drug use, associated with a loss of control over consumption, leading to craving. When consumption is stopped, withdrawal symptoms may emerge: a negative emotional state, cognitive problems and physical symptoms with some products (alcohol and opiates, for example). Relapse episodes may occur during this withdrawal period, countering the negative effects of withdrawal. Relapse episodes can also be observed after long periods of abstinence. They can be precipitated by re-exposure to the context in which the drugs were taken, or by stress. Regardless of the stage of addiction (e.g., development of the addictive behavior, or relapse) changes in brain function and structure can be observed. Some brain structures are therefore modified, such as the prefrontal cortex, where several neuroadaptations have been identified. Some of these changes are described in this paper.

Air pollution is the main urban-related environmental hazard and one of the major contributors to the global burden of disease based on its cardiovascular-respiratory impacts. In children, exposure to urban air pollution is associated, among others, with decelerated neurodevelopment early in life and increased risk of neurodevelopmental problems such as attention-deficit hyperactivity disorder, autism spectrum disorders, academic failure and the start of Alzheimer's pathogenesis. However, the evidence of the effects of air pollution on brain development is still inadequate, mainly due to the limitations in (a) characterizing brain development (most studies were based on subjective tools such as questionnaires or neuropsychological tests) and (b) air pollution exposure (most studies only used residential levels based on geographical modelling and also overlooking the variation in the mixture of air pollutants as well as the composition and hence toxicity of particulate pollutants in different settings), (c) the lack of studies during the most vulnerable stages of brain development (foetal and early life (first two years post-natally)) and (d) the lack of structural and functional imaging data underlying these effects. In mice, in utero exposure to fine particles was linked to structural brain changes and there is a need to establish the generalizability of these findings in human beings. Though scarce, current evidence in children supports the importance of the pre-natal period as a susceptible window of exposure. Two studies in schoolchildren found that pre-natal air pollution exposure might damage brain structure while exposure during childhood was not linked to any structural alteration. Another study showed that children with higher traffic-related air pollution at school had lower functional integration in key brain networks, but no changes in brain structure, possibly partly because of the time window of air pollution exposure (in utero versus childhood exposure). A key development is to discover the windows of greatest sensitivity of structural brain changes to air pollution exposure by incorporating the recent advances in non-invasive imaging to characterize natal and post-natal brain development and exploring whether and to what extend placental dysfunction could mediate such an association. Studying pre-natal life is important because effects at this time are of a potentially irreversible nature and because the largest preventive opportunities occur during these periods.

Gray matters: ViT-GAN framework for identifying schizophrenia biomarkers linking structural MRI and functional network connectivity