Neurobiological Profiles Research Articles

Advancing Alzheimer's Treatment: Unleashing the Power of Donanemab and Quantum Computing for Enhanced Patient Outcomes

Donanemab is the first antibody to target pyroglutamate-modified amyloid-beta in Alzheimer's disease selectively; thus, it represents a significant breakthrough in disease-modifying treatments. Importantly, its mechanism of action encourages adequate clearance of plaques and does not even worsen outcomes for early-stage patients, in contrast to previous treatments that did not promote clearing for plaques or even worsened the outcomes of early-stage patients. The integration of quantum computing in drug discovery holds tremendous transformations in terms of enhancing the therapeutic approach against Alzheimer's disease. Researchers can speed up discovering novel compounds, optimize treatment regimens, and personalize patient care according to individual neurobiological profiles by using quantum computing powers. The letter to the editor discusses the unique attributes of Donanemab, its clinical superiority, and the related side effects, besides pushing for the promising future of integrating quantum computing into the paradigms of Alzheimer's treatment. Though promising, integrating quantum computing into medical practice is challenged by factors such as high computational costs, data privacy, and ethical considerations that must be taken within strict regulatory frameworks.

Perspectives on Integrating Biological Assessments to Address the Health Effects of Childhood Adversities.

A majority of adults in the United States (US) report a range of stressful and potentially traumatic childhood experiences (e.g., physical or sexual abuse, witnessing violence, neglect). Such adversities are associated with a range of mental (e.g., anxiety, mood, and behavioral difficulties) and physical (e.g., cardiovascular illnesses, diabetes, asthma) health problems. Increasingly, precision medicine approaches seek to prevent and treat such multifinal downstream health problems by identifying common etiological pathways (e.g., inflammation and immune pathways) and candidate biomarkers to target interventions. In this context, we review the rationale for continued research to identify biomarkers of childhood adversity. Building on the bioecological theory, we emphasize that individual neurobiological profiles develop within multiple ecological levels (individual, family, neighborhood, macrosocial) that confer both risk and protective factors that can attenuate or amplify biological effects of childhood adversity. Given the limited data on adversity-associated biomarkers for children and adolescents, we discuss future recommendations for research, implications for clinical care, and ethical considerations. Preventing childhood adversity and supporting adversity- and trauma-informed systemic intervention approaches remains our primary recommendation. We highlight the continued need to consider both biomarkers of risk and protective factors across ecological levels in future research.

Co‐methylation network analysis of Psychosis in Alzheimer’s disease

AbstractBackgroundPsychosis (broadly delusions and hallucinations) has a cumulative disease prevalence of around 40% in Alzheimer’s disease (AD). The epigenomic, genomic, and neuropathological data provide powerful evidence that AD+P has a distinct neurobiological profile. Here, we used the weighted gene co‐expression network analysis (WGCNA) method to investigate DNA methylation associated with AD+P in the dorsolateral prefrontal cortex of 153 post‐mortem brain samples.MethodOur primary analysis focused on applying WGCNA to the PITT‐ADRC cohort, followed by subsequent replication of its findings in the BDR cohort. The genotype data from PITT‐ADRC and the WGCNA results were further utilized to identify the most significant methylation Quantitative Trait Loci (mQTLs) associated with psychosis. Subsequently, we explored RNA sequencing data from PITT‐ADRC to identify genes affected by the replicated findings uncovered in our primary analysis.ResultWe identified five AD+P‐related modules in the PITT‐ADRC cohort, with one of them being replicated in the BDR cohort. This replicated AD+P‐related module exhibits a high enrichment in the T cell receptor signalling pathway. According to the colocalization analysis results, this module shares significant SNPs in some regions that are also significantly associated with Schizophrenia and Educational Attainment.ConclusionUnderstanding molecular differences between AD and Psychosis at the genetic and epigenetic levels could guide us in discovering appropriate treatments for AD+P cases. To this end, we initiated a comprehensive, large sample‐sized network analysis study based on genetic and epigenetic data.

Subtype‐specific patterns of tau pathology in Alzheimer’s and related disorders

AbstractBackgroundAlzheimer disease (AD) involves neurodegenerative disorders with progressive cognitive decline. Atypical presentations like Posterior Cortical Atrophy (PCA) and Logopenic Variant Primary Progressive Aphasia (lvPPA) exhibit distinct clinical profiles. PCA affects the posterior parietal and occipital lobes, causing visuospatial deficits, while lvPPA manifests as language impairment in the temporoparietal region. Understanding the biological underpinnings of these variants is crucial for deciphering AD’s heterogeneity.MethodParticipants diagnosed with AD dementia (n = 54, female = 25, Age: 75.23±6.52), PCA (n = 9, female = 8, Age: 62.78±7.21), and lvPPA (n = 6, female = 2, Age: 66.33±6.38) from the Knight Alzheimer Disease Research Center (Knight ADRC) underwent 18F‐AV‐1451 tau‐PET imaging. Tau deposition, along with nine biological properties, was mapped to the cortical surface (Figure 1A): gene expression, myelin, cortical thickness, sensorimotor association axis, evolutionary expansion, cerebral blood flow (CBF), cerebral blood volume (CBV), and cerebral metabolic rate of glucose (CMRglu) (Figure 1B). Correlation matrices and generalized linear models (GLMs) assessed relationships between tau accumulation and biological properties.ResultA correlation matrix (Figure 2A) shows significant positive associations (p<0.05) between evolutionary expansion patterns and tau accumulation in AD (r = 0.53), PCA (r = 0.29), and lvPPA (r = 0.56); and gene expression in PCA (r = 0.51). Conversely, strongest negative associations were observed in AD (r = ‐0.38, r = ‐0.15) and lvPPA (r = ‐0.18, r = ‐0.28) for CBF and myelin mapping, respectively, and in PCA (r = ‐0.25, ‐0.23) for cortical thickness and sensorimotor association axis. GLMs demonstrated significant relationships between cerebrovascular health and evolutionary expansion with tau measures across all groups. AD (r = ‐0.52) and PCA (r = ‐0.19) exhibited negative associations with gene expression and myelin mapping, respectively. Additionally, lvPPA (r = 0.39) displayed positive association with the sensorimotor association cortex.ConclusionResults elucidate distinct tau deposition patterns in AD, PCA, and lvPPA, providing insights into subtype‐specific pathophysiology. The correlation matrix and GLMs highlight the significance of evolutionary expansion and cerebrovascular health in tau accumulation. Associations underscore the complex interplay of gene expression, myelin mapping, and cortical thickness with tau pathology. Findings contribute to understanding heterogeneity within AD spectrum disorders, emphasizing the multifaceted nature of neurodegenerative processes. Further research promises refined diagnostic and therapeutic strategies tailored to distinct neurobiological profiles in AD, PCA, and lvPPA.

Borderline personality disorder and post-traumatic stress disorder in adolescents: protocol for a comparative study of borderline personality disorder with and without comorbid post-traumatic stress disorder (BORDERSTRESS-ADO)

BackgroundBorderline Personality Disorder (BPD) is a prevalent and debilitating psychiatric condition often accompanied by Post-Traumatic Stress Disorder (PTSD), with a substantial prevalence of trauma history among affected individuals. The clinical, cognitive, and cerebral parallels shared with PTSD suggest a trauma-related etiology for BPD. Studies consistently demonstrate a reduction in hippocampal volume in individuals with BPD, echoing findings in PTSD. However, the interpretation of this shared neurobiological profile remains contentious, with ongoing debates regarding the independence of these pathologies or the potential exacerbation of diminished hippocampal volume in BPD due to concurrent PTSD. Differential impacts on hippocampal subfields across both disorders may further complicate interpretation, suggesting the volume of hippocampal subfields as a potential discriminant biomarker. This study aims to characterize the multidimensional specific and shared profiles of BPD and PTSD-related alterations, with a particular emphasis on hippocampal subfields during adolescence, a crucial period in BPD development.MethodsThis study focuses on female adolescents, who are more prevalent in the BPD population. Participants are categorized into three groups: BPD, BPD with comorbid PTSD, and a control group of matched healthy individuals. Data collection encompasses clinical, cognitive, and neuroimaging domains commonly affected in both disorders, utilizing various imaging markers (including gray matter macrostructure, white matter microstructural integrity, and regional functional connectivity).DiscussionThis study examines adolescent BPD with and without comorbid PTSD on clinical, neuroimaging, and cognitive levels. It is the first to use a comprehensive multi-modal approach within the same sample. Additionally, it uniquely explores hippocampal subfield volume differences in adolescents. Analysis of the relationship between the investigated domains and the effects of PTSD comorbidity will elucidate specific and shared alteration profiles in both disorders.Trial registrationIDRCB number 2019-A00366-51 / clinicaltrials.gov ID: NCT0485274. Registered on 21/04/2021.

Shared and distinct prefrontal cortex alterations of implicit emotion regulation in depression and anxiety: An fNIRS investigation

Emotion regulation deficits, particularly in cognitive reappraisal, are crucial in depression and anxiety. However, research on the neural mechanisms of implicit emotion regulation is lacking, and it remains unclear whether these mechanisms are shared or distinct between the two disorders. We investigated the neural mechanisms of implicit cognitive reappraisal in 28 individuals with major depressive disorder (MDD), 25 with generalized anxiety disorder (GAD), and 30 healthy controls (HC) using functional near-infrared spectroscopy (fNIRS). Participants completed an implicit cognitive reappraisal task and underwent neuropsychological and clinical assessments. We found that MDD patients reported higher levels of rumination and lower utilization of cognitive reappraisal, while GAD patients reported reduced use of perspective-taking. Notably, both MDD and GAD patients exhibited decreased activation in the dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex (OFC) compared to HC participants during implicit cognitive reappraisal. Specifically, inadequate OFC activation was observed in MDD patients, while GAD patients demonstrated OFC deactivation during the task. Furthermore, DLPFC activation showed a negative correlation with depression severity in MDD patients, while OFC activation was positively correlated with perspective-taking in GAD patients. fNIRS has limited depth and spatial resolution. Our fNIRS study is the first to reveal shared and distinct neurobiological profiles of depression and anxiety in implicit emotion regulation. These findings underscore the significance of reduced DLPFC/OFC activation in emotion regulation impairment and highlight unique OFC activation patterns in these disorders. These insights have potential implications for developing cognitive-behavioral therapy and transcranial magnetic stimulation as treatment approaches.

HHC-induced psychosis: a case series of psychotic illness triggered by a widely available semisynthetic cannabinoid.

Use of both cannabis and synthetic cannabinoids has been regularly linked to the development of psychotic illness. Thus, semisynthetic cannabinoids such as hexahydrocannabinol (HHC), which have a similar neurobiological profile to delta-9-THC, may also be expected to lead to psychotic illness. However, no such relationship has yet been reported in scientific literature. HHC is readily available online and in many vape shops in Ireland. Here, we present two cases of psychotic illness which appear to have been precipitated by use of legally purchased HHC and discuss its psychotogenic role and factors linked to its current widespread availability.

Understanding Wellbeing Profiles According to White Matter Structural Connectivity Sub-types in Early Adolescents: The First Hundred Brains Cohort from the Longitudinal Adolescent Brain Study

Wellbeing is protective against the emergence of psychopathology. Neurobiological markers associated with mental wellbeing during adolescence are important to understand. Limited research has examined neural networks (white matter tracts) and mental wellbeing in early adolescence specifically. A cross-sectional diffusion tensor imaging analysis approach was conducted, from the Longitudinal Adolescent Brain study, First Hundred Brains cohort (N = 99; 46.5% female; Mage = 13.01, SD = 0.55). Participants completed self-report measures including wellbeing, quality-of-life, and psychological distress. Potential neurobiological profiles using fractional anisotropy, axial, and radial diffusivity were determined via a whole brain voxel-wise approach, and hierarchical cluster analysis of fractional anisotropy values, obtained from 21 major white matter tracts. Three cluster groups with significantly different neurobiological profiles were distinguished. No significant differences were found between the three cluster groups and measures of wellbeing, but two left lateralized significant associations between white matter tracts and wellbeing measures were found. These results provide preliminary evidence for potential neurobiological markers of mental health and wellbeing in early adolescence and should be tracked longitudinally to provide more detailed and robust findings.

15. Heterogeneity in Depression: Evidence for Distinct Clinical and Neurobiological Profiles

15. Heterogeneity in Depression: Evidence for Distinct Clinical and Neurobiological Profiles

Cross-sectional and longitudinal neuroanatomical profiles of distinct clinical (adaptive) outcomes in autism.

Individuals with autism spectrum disorder (henceforth referred to as autism) display significant variation in clinical outcome. For instance, across age, some individuals' adaptive skills naturally improve or remain stable, while others' decrease. To pave the way for 'precision-medicine' approaches, it is crucial to identify the cross-sectional and, given the developmental nature of autism, longitudinal neurobiological (including neuroanatomical and linked genetic) correlates of this variation. We conducted a longitudinal follow-up study of 333 individuals (161 autistic and 172 neurotypicalindividuals, aged 6-30 years), with two assessment time points separated by ~12-24 months. We collected behavioural (Vineland Adaptive Behaviour Scale-II, VABS-II) and neuroanatomical (structural magnetic resonance imaging) data. Autistic participants were grouped into clinically meaningful "Increasers", "No-changers", and "Decreasers" in adaptive behaviour (based on VABS-II scores). We compared each clinical subgroup's neuroanatomy (surface area and cortical thickness at T1, ∆T (intra-individual change) and T2) to that of the neurotypicals. Next, we explored the neuroanatomical differences' potential genomic associates using the Allen Human Brain Atlas. Clinical subgroups had distinct neuroanatomical profiles in surface area and cortical thickness at baseline, neuroanatomical development, and follow-up. These profiles were enriched for genes previously associated with autism and for genes previously linked to neurobiological pathways implicated in autism (e.g. excitation-inhibition systems). Our findings suggest that distinct clinical outcomes (i.e. intra-individual change in clinical profiles) linked to autism core symptoms are associated with atypical cross-sectional and longitudinal, i.e. developmental, neurobiological profiles. If validated, our findings may advance the development of interventions, e.g. targeting mechanisms linked to relatively poorer outcomes.

Type of Trauma Exposure Impacts Neural Reactivity to Errors

Abstract: Studies suggest that individuals with a history of trauma exposure display abnormal reactivity to threat, though the pattern of findings across prior studies has been inconsistent. At least two factors likely contribute to previous discrepant findings: (1) the type of index trauma event and (2) the type of threat paradigm. Accordingly, the current study aimed to examine the impact of trauma type on a specific psychophysiological index of threat sensitivity – error negativity (Ne), also described as error-related negativity (ERN). Young adults were classified into three groups: lifetime history of interpersonal trauma (i.e., sexual assault, physical assault, or immediate family violence; n = 30), lifetime history of a non-interpersonal trauma (e.g., accidents, natural disasters; n = 30), or no lifetime history of trauma ( n = 64). All participants completed a well-validated flanker task designed to elicit the Ne/ERN during continuous electroencephalographic (EEG) data collection. Results indicated that individuals with non-interpersonal trauma exposure displayed reduced Ne/ERN amplitude compared with the other two groups (who did not differ from each other). Broadly, these findings highlight the importance of trauma type and theory suggesting different forms of trauma may result in different neurobiological profiles. These findings also add to a growing literature indicating that non-interpersonal traumas may be uniquely associated with blunted threat sensitivity and deficiencies in self-monitoring.

Characterizing different cognitive and neurobiological profiles in a community sample of children using a non-parametric approach: An fMRI study

Executive Functions (EF) is an umbrella term for a set of mental processes geared towards goal-directed behavior supporting academic skills such as reading abilities. One of the brain's functional networks implicated in EF is the Default Mode Network (DMN). The current study uses measures of inhibitory control, a main sub-function of EF, to create cognitive and neurobiological "inhibitory control profiles" and relate them to reading abilities in a large sample (N=5055) of adolescents aged 9-10 from the Adolescent Brain Cognitive Development (ABCD) study. Using a Latent Profile Analysis (LPA) approach, data related to inhibitory control was divided into four inhibition classes. For each class, functional connectivity within the DMN was calculated from resting-state data, using a non-parametric algorithm for detecting group similarities. These inhibitory control profiles were then related to reading abilities. The four inhibitory control groups showed significantly different reading abilities, with neurobiologically different DMN segregation profiles for each class versus controls. The current study demonstrates that a community sample of children is not entirely homogeneous and is composed of different subgroups that can be differentiated both behaviorally/cognitively and neurobiologically, by focusing on inhibitory control and the DMN. Educational implications relating these results to reading abilities are noted.

Free-Water Diffusion Magnetic Resonance Imaging Differentiates Suicidal Ideation From Suicide Attempt in Treatment-Resistant Depression

Suicide attempt is highly prevalent in treatment-resistant depression (TRD); however, the neurobiological profile of suicidal ideation versus suicide attempt is unclear. Neuroimaging methods including diffusion magnetic resonance imaging-based free-water imaging may identify neural correlates underlying suicidal ideation and attempts in individuals with TRD. Diffusion magnetic resonance imaging data were obtained from 64 male and female participants (mean age 44.5 ± 14.2 years), including 39 patients with TRD (n= 21 and lifetime history of suicidal ideation but no attempts [SI group]; n= 18 with lifetime history of suicide attempt [SA group]), and 25 age- and sex-matched healthy control participants. Depression and suicidal ideation severity were examined using clinician-rated and self-report measures. Whole-brain neuroimaging analysis was conducted using tract-based spatial statistics via FSL to identify differences in white matter microstructure in the SI versus SA groups and in patients versus control participants. Free-water imaging revealed elevated axial diffusivity and extracellular free water in fronto-thalamo-limbic white matter tracts of the SA group compared with the SI group. In a separate comparison, patients with TRD had widespread reductions in fractional anisotropy and axial diffusivity, as well as elevated radial diffusivity compared with control participants (thresholded p < .05, familywise error corrected). A unique neural signature consisting of elevated axial diffusivity and free water was identified in patients with TRD and suicide attempt history. Findings of reduced fractional anisotropy, axial diffusivity, and elevated radial diffusivity in patients versus control participants are consistent with previously published studies. Multimodal and prospective investigations are recommended to better understand biological correlates of suicide attempt in TRD.

A Neurobiological Profile Underlying Comorbidity Load and Prospective Increases in Dysphoria in a Focal Fear Sample

Knowledge of the neural mechanisms underlying increased disease burden in anxiety disorders that is unaccounted for by individual categorical diagnoses could lead to improved clinical care. Here, we tested the utility of a joint functional magnetic resonance imaging-electroencephalography neurobiological profile characterized by overvaluation of negative stimuli (amygdala) in combination with blunted elaborated processing of these same stimuli (the late positive potential [LPP], an event-related potential) in predicting increased psychopathology across a 2-year period in people with anxiety disorders. One hundred ten participants (64 female, 45 male, 1 other) including 78 participants with phobias who varied in the extent of their internalizing comorbidity and 32 participants who were free from psychopathology viewed negative and neutral pictures during separate functional magnetic resonance imaging blood oxygen level-dependent and electroencephalogram recordings. Dysphoria was assessed at baseline and 2 years later. Participants with both heightened amygdala activation and blunted LPPs to negative pictures showed the greatest increases in dysphoria 2 years later. Cross-sectionally, participants with higher comorbidity load (≥2 additional diagnoses, n= 34) showed increased amygdala activation to negative pictures compared with participants with lower comorbidity load (≤1 additional diagnosis, n= 44) and compared with participants free from psychopathology. In addition, high comorbid participants showed reduced LPPs to negative pictures compared with low comorbid participants. Heightened amygdala in response to negative stimuli in combination with blunted LPPs could indicate overvaluation of threatening stimuli in the absence of elaborated processing that might otherwise help regulate threat responding. This brain profile could underlie the worsening and maintenance of internalizing psychopathology over time.

Crosstalk between Schizophrenia and Metabolic Syndrome: The Role of Oxytocinergic Dysfunction.

The high prevalence of metabolic syndrome in persons with schizophrenia has spurred investigational efforts to study the mechanism beneath its pathophysiology. Early psychosis dysfunction is present across multiple organ systems. On this account, schizophrenia may be a multisystem disorder in which one organ system is predominantly affected and where other organ systems are also concurrently involved. Growing evidence of the overlapping neurobiological profiles of metabolic risk factors and psychiatric symptoms, such as an association with cognitive dysfunction, altered autonomic nervous system regulation, desynchrony in the resting-state default mode network, and shared genetic liability, suggest that metabolic syndrome and schizophrenia are connected via common pathways that are central to schizophrenia pathogenesis, which may be underpinned by oxytocin system dysfunction. Oxytocin, a hormone that involves in the mechanisms of food intake and metabolic homeostasis, may partly explain this piece of the puzzle in the mechanism underlying this association. Given its prosocial and anorexigenic properties, oxytocin has been administered intranasally to investigate its therapeutic potential in schizophrenia and obesity. Although the pathophysiology and mechanisms of oxytocinergic dysfunction in metabolic syndrome and schizophrenia are both complex and it is still too early to draw a conclusion upon, oxytocinergic dysfunction may yield a new mechanistic insight into schizophrenia pathogenesis and treatment.

Distinctive Effects of Modafinil and Caffeine on the Regional Expression of Histone Deacetylases in the Brain

Psychostimulants produce different behavioral and neurobiological profiles. For example, some stimulants cause neuroplastic changes leading to addiction and cognitive deficits while others enhance cognition. Epigenetic mechanisms are known contributory factors to drug-induced neuroadaptations. These epigenetic changes include dysregulation of histone deacetylases (HDACs) proposed to participate in maintaining aberrant transcriptional programs associated with altered cognitive functions and behaviors.

Beyond DSM Criteria: Neurobiological and Treatment Implications of Clinically-Identifiable Phenotypes of Late-Life Depression

<h2>Abstract</h2> The diagnosis of Major Depressive Disorder in older adults follows the same DSM5 criteria as is used in younger populations. However, this conceptualization limits us to clinical phenomenology as seen in younger populations. It is informed neither by contributory and comorbid aging processes nor by modern behavioral concepts with a specific underlying neurobiology. Such processes vary across the population of older depressed adults yet can influence short- and long-term clinical outcomes and may have prognostic value. Examples of aging processes include changes in cognitive performance but also extend to motor function, sensory deprivation, and fatigue. Behavioral markers with distinct neurobiological profiles include alterations in reward processes such as the development of apathy, as well as comorbid rumination, anxiety, worry and sleep disturbances. This symposium will discuss how aging processes and deeper assessments of behavioral symptom markers may present in and contribute to negative outcomes for patients with late-life depression (LLD). Dr. Bret Rutherford will discuss the role of motor and gait slowing in older adults. He will discuss how this common finding may influence the development of and presentation of LLD. He will also present a scientific model of how this may reflect underlying dysfunction of dopamine neurotransmitter systems. Dr. Sarah Szymkowicz will discuss work examining profiles of cognitive performance in patients will LLD. She will present data on how different cognitive performance profiles are related to demographic differences, clinical presentation, and how they may be related to acute treatment outcomes. Dr. Lauren Oberlin will then discuss the occurrence of apathy in LLD. She will review the clinical implications of apathy in this population and then present data from a neuroimaging study detailing the discrete functional imaging findings associated with this behavioral marker. Finally, Dr. Warren Taylor will present data from a recently completed pharmacoimaging study that includes clinical deep symptom phenotyping of patients with LLD, including apathy, rumination, and fatigue. He will discuss how different behavioral measures are associated with demographic differences yet also are related to differences in cognitive performance and functional disability. He will also present how these symptoms change during treatment with a selective serotonin reuptake inhibitor and how they may influence the overall antidepressant effect. The session will conclude with an open discussion involving the audience about how to integrate these findings and how they can inform clinical practice. This symposium will highlight the scientific need to do what many clinicians are already doing – conceptualizing LLD beyond traditional depressive symptoms. New approaches that embrace clinical heterogeneity with a broader conceptualization of the presentation of LLD have the potential to provide better prognostic information and identify new targets for pharmacological and non-pharmacological interventions.

Characterizing cerebral metabolite profiles in anorexia and bulimia nervosa and their associations with habitual behavior

Anorexia nervosa (AN) and bulimia nervosa (BN) are associated with altered brain structure and function, as well as increased habitual behavior. This neurobehavioral profile may implicate neurochemical changes in the pathogenesis of these illnesses. Altered glutamate, myo-inositol and N-acetyl aspartate (NAA) concentrations are reported in restrictive AN, yet whether these extend to binge-eating disorders, or relate to habitual traits in affected individuals, remains unknown. We therefore used single-voxel proton magnetic resonance spectroscopy to measure glutamate, myo-inositol, and NAA in the right inferior lateral prefrontal cortex and the right occipital cortex of 85 women [n = 22 AN (binge-eating/purging subtype; AN-BP), n = 33 BN, n = 30 controls]. To index habitual behavior, participants performed an instrumental learning task and completed the Creature of Habit Scale. Women with AN-BP, but not BN, had reduced myo-inositol and NAA concentrations relative to controls in both regions. Although patient groups had intact instrumental learning task performance, both groups reported increased routine behaviors compared to controls, and automaticity was related to reduced prefrontal glutamate and NAA participants with AN-BP. Our findings extend previous reports of reduced myo-inositol and NAA levels in restrictive AN to AN-BP, which may reflect disrupted axonal-glial signaling. Although we found inconsistent support for increased habitual behavior in AN-BP and BN, we identified preliminary associations between prefrontal metabolites and automaticity in AN-BP. These results provide further evidence of unique neurobiological profiles across binge-eating disorders.

Prefrontal cortex alterations in major depressive disorder, generalized anxiety disorder and their comorbidity during a verbal fluency task assessed by multi-channel near-infrared spectroscopy

Major depressive disorder (MDD) and generalized anxiety disorder (GAD) are frequently comorbid with each other, and both associated with substantial cognitive impairments; however, it is still unclear whether their impairments are neurobiologically similar or distinct. This study aims to investigate the cognitive functions of the prefrontal cortex (PFC) in patients with MDD and GAD during the verbal fluency task (VFT) using functional near-infrared spectroscopy (fNIRS). Fifty-two patients with MDD, fifty-one patients with GAD, fifty-two patients with the comorbidity of MDD and GAD (CMG), and forty-seven healthy controls (HC) participated in the study. Significant hypoactivation in the left ventrolateral and the left dorsolateral PFC was common in all patient groups when compared to HCs, suggesting a shared etiology. Furthermore, MDD patients showed significant hypoactivation at the right frontal pole cortex (FPoC) when compared to HCs and significant hypoactivation at the middle FPoC when compared to the CMG patients. Our work is the first fNIRS study to reveal the shared and unique neurobiological profiles of MDD, GAD and their comorbidity under the same standard experimentation condition, suggesting fNIRS holds promise as an adjutant to assist clinical diagnosis.

Clinical evidence in sexual orientations: definitions, neurobiological profiles, and psychological implications

Educating the population in the field of mental health includes a set of educational, upbringing, agitation and propaganda activities aimed at promoting a healthy lifestyle, preventing diseases, maintaining and strengthening health, increasing the ability of people to work, and prolonging their active life.