Search

Background and Aims: The brain age gap (BAG), calculated as the difference between a machine learning model‐based predicted brain age and chronological age, has been increasingly investigated in psychiatric disorders. Tobacco and alcohol use are associated with increased BAG; however, no studies have compared global and regional BAG across substances other than alcohol and tobacco. This study aimed to compare global and regional estimates of brain age in individuals with substance use disorders and healthy controls. Design: This was a cross‐sectional study. Setting: This is an Enhancing Neuro Imaging through Meta‐Analysis Consortium (ENIGMA) Addiction Working Group study including data from 38 global sites. Participants: This study included 2606 participants, of whom 1725 were cases with a substance use disorder and 881 healthy controls. Measurements: This study used the Kaufmann brain age prediction algorithms to generate global and regional brain age estimates using T1 weighted magnetic resonance imaging (MRI) scans. We used linear mixed effects models to compare global and regional (FreeSurfer lobestrict output) BAG (i.e. predicted minus chronological age) between individuals with one of five primary substance use disorders as well as healthy controls. Findings Alcohol use disorder (β = −5.49, t = −5.51, p < 0.001) was associated with higher global BAG, whereas amphetamine‐type stimulant use disorder (β = 3.44, t = 2.42, p = 0.02) was associated with lower global BAG in the separate substance‐specific models. Conclusions: People with alcohol use disorder appear to have a higher brain‐age gap than people without alcohol use disorder, which is consistent with other evidence of the negative impact of alcohol on the brain. [ABSTRACT FROM AUTHOR]

Background: Shifts in peak frequencies of oscillatory neural rhythms are put forward as a principal mechanism by which cross‐frequency coupling/decoupling is implemented in the brain. During active neural processing, functional integration is facilitated through transitory formations of "harmonic" cross‐frequency couplings, whereas "nonharmonic" decoupling among neural oscillatory rhythms is postulated to characterize the resting, default state of the brain, minimizing the occurrence of spurious, noisy, background couplings. Methods: Within this exploratory, randomized, placebo‐controlled trial, we assessed whether the transient occurrence of nonharmonic and harmonic relationships between peak‐frequencies in the alpha (8–14 Hz) and theta (4–8 Hz) bands is impacted by intranasal administration of oxytocin, a neuromodulator implicated in improving homeostasis and reducing stress/anxiety. To do so, resting‐state electroencephalography was acquired before and after 4 weeks of oxytocin administration (12 IU twice‐daily) in children with autism spectrum disorder (8–12 years, n = 33 oxytocin; n = 34 placebo). At the baseline, neural assessments of children with autism were compared with those of a matched cohort of children without autism (n = 40). Results: Compared to nonautistic peers, autistic children displayed a lower incidence of nonharmonic alpha‐theta cross‐frequency decoupling, indicating a higher incidence of spurious "noisy" coupling in their resting brain (p =.001). Dimensionally, increased neural coupling was associated with more social difficulties (p =.002) and lower activity of the parasympathetic "rest & digest" branch of the autonomic nervous system (p =.018), indexed with high‐frequency heart‐rate‐variability. Notably, after oxytocin administration, the transient formation of nonharmonic cross‐frequency configurations was increased in the cohort of autistic children (p <.001), indicating a beneficial effect of oxytocin on reducing spurious cross‐frequency‐interactions. Furthermore, parallel epigenetics changes of the oxytocin receptor gene indicated that the neural effects were likely mediated by changes in endogenous oxytocinergic signaling (p =.006). Conclusions: Chronic oxytocin induced important homeostatic changes in the resting‐state intrinsic neural frequency architecture, reflective of reduced noisy oscillatory couplings and improved signal‐to‐noise properties. [ABSTRACT FROM AUTHOR]

Enactivism is a branch of embodied cognition theory that argues for a highly distributed model of cognition as a sense‐making process involving brain, body, environment, and subjective experience. It is a theoretical framework with potential value for nursing since it offers an integrated framework for human sense‐making that includes physiological and psychological factors as well as the primary experience of subjective perceptions. This paper presents an introduction to the background and main tenets of enactivist theory. These are discussed in relation to nursing, and mental health nursing to argue for the relevance of enactivism in nursing knowledge. [ABSTRACT FROM AUTHOR]

Summary: Acute caffeine intake affects brain and cardiovascular physiology, yet the concentration–effect relationships on the electroencephalogram and cardiac autonomic activity during sleep are poorly understood. To tackle this question, we simultaneously quantified the plasma caffeine concentration with ultra‐high‐performance liquid chromatography, as well as the electroencephalogram, heart rate and high‐frequency (0.15–0.4 Hz) spectral power in heart rate variability, representing parasympathetic activity, with standard polysomnography during undisturbed human sleep. Twenty‐one healthy young men in randomized, double‐blind, crossover fashion, ingested 160 mg caffeine or placebo in a delayed, pulsatile‐release caffeine formula at their habitual bedtime, and initiated a 4‐hr sleep opportunity 4.5 hr later. The mean caffeine levels during sleep exhibited high individual variability between 0.2 and 18.4 μmol L−1. Across the first two non‐rapid‐eye‐movement (NREM)–rapid‐eye‐movement sleep cycles, electroencephalogram delta (0.75–2.5 Hz) activity and heart rate were reliably modulated by waking and sleep states. Caffeine dose‐dependently reduced delta activity and heart rate, and increased high‐frequency heart rate variability in NREM sleep when compared with placebo. The average reduction in heart rate equalled 3.24 ± 0.77 beats per minute. Non‐linear statistical models suggest that caffeine levels above ~7.4 μmol L−1 decreased electroencephalogram delta activity, whereas concentrations above ~4.3 μmol L−1 and ~ 4.9 μmol L−1, respectively, reduced heart rate and increased high‐frequency heart rate variability. These findings provide quantitative concentration–effect relationships of caffeine, electroencephalogram delta power and cardiac autonomic activity, and suggest increased parasympathetic activity during sleep after intake of caffeine. [ABSTRACT FROM AUTHOR]

The brain is essential for processing and integrating sensory signals coming from peripheral tissues. Conversely, the autonomic nervous system regulated by brain centres modulates the immune responses involved in the genesis and progression of cardiovascular diseases. Understanding the pathophysiological bases of this relationship established between the brain and immune system is relevant for advancing therapies. An additional mechanism involved in the regulation of cardiovascular function is provided by the brain‐mediated control of the renin–angiotensin system. In both cases, the communication is typically bidirectional and established by afferent and sensory signals collected at the level of peripheral tissues, efferent circuits, as well as of hormones. Understanding how the brain mediates the bidirectional communication and how the immune system participates in this process is object of intense investigation. This review examines key findings that support a role for these interactions in the pathogenesis of major vascular diseases that are characterized by a consistent alteration of the immune response, such as hypertension and atherosclerosis. In addition, we provide a critical appraisal of the translational implications that these discoveries have in the clinical setting where an effective management of neuroimmune and/or neuroinflammatory state might be beneficial. [ABSTRACT FROM AUTHOR]

Objective: Adults with binge‐eating disorder (BED), compared with those without BED, demonstrate higher blood‐oxygen–level‐dependent (BOLD) response to food cues in reward‐related regions of the brain. It is not known whether cognitive behavioral therapy (CBT) can reverse this reward system hyperactivation. This randomized controlled trial (RCT) assessed changes in BOLD response to binge‐eating cues following CBT versus wait‐list control (WLC). Method: Females with BED (N = 40) were randomized to CBT or WLC. Participants completed assessments at baseline and 16 weeks including measures of eating and appetite and functional magnetic resonance imaging (fMRI) to measure BOLD response while listening to personalized scripts of binge‐eating and neutral‐relaxing cues. Data were analyzed using general linear models with mixed effects. Results: Overall retention rate was 87.5%. CBT achieved significantly greater reductions in binge‐eating episodes than WLC (mean ± standard error decline of 14.6 ± 2.7 vs. 5.7 ± 2.8 episodes in the past 28 days, respectively; p = 0.03). CBT and WLC did not differ significantly in changes in neural responses to binge‐eating stimuli during the fMRI sessions. Compared with WLC, CBT had significantly greater improvements in reward‐based eating drive, disinhibition, and hunger as assessed by questionnaires (ps < 0.05). Discussion: CBT was effective in reducing binge eating, but, contrary to our hypothesis, CBT did not improve BOLD response to auditory binge‐eating stimuli in reward regions of the brain. Further studies are needed to assess mechanisms underlying improvements with CBT for BED. Trial Registration: ClinicalTrials.gov identifier: NCT03604172 [ABSTRACT FROM AUTHOR]

Background: Despite the increased risk for people with an intellectual disability developing dementia, post‐diagnostic psychosocial supports such as cognitive stimulation therapy (CST) are not routinely offered and there is limited research examining this intervention with people with intellectual disabilities. The aim of this study was to explore the feasibility of CST for older adults with intellectual disability to support active ageing. Methods: Five client participants attended a 14‐session CST group and four staff attended a focus group. Reflexive thematic analysis was used to investigate the client and staff narratives. Results: Three key themes were generated: (1) Brain Health, (2) Connecting with others, and (3) Barriers and Enablers. Conclusion: Findings indicated the suitability of CST as a way of supporting active ageing for older adults with intellectual disability. This study adds to the growing knowledge about service provision for older adults and their changing needs as they age and identifies clinical implications such as staff training to support intervention adherence. [ABSTRACT FROM AUTHOR]

Background: Numerous studies have investigated the potential effects of transcranial direct current stimulation (tDCS) on improving symptoms related to Alzheimer's disease (AD). However, these studies have produced inconsistent results, leading to a need for further investigation. Methods: A comprehensive search was conducted, including articles published from the initial availability date to 5 April 2024. The extracted study data were analyzed using STATA 12.0 software. The standard mean difference (SMD) and a 95% confidence interval (CI) were calculated to assess the effects of tDCS. Results: A total of 18 studies assessing the effects of tDCS on AD were included in the study. The study revealed that tDCS has an immediate positive impact on general cognitive, executive, language, and visuospatial function. However, the study did not observe any other significant effect of tDCS treatment on improvements in brain function, including long‐term effects on general cognitive, attention, language, and memory function, as well as immediate effects on attention and memory function. Conclusions: In conclusion, the study suggests that tDCS may be a promising intervention for improving the cognitive function of patients with AD. However, given the complex and multifactorial nature of AD, further well‐designed studies with larger sample sizes are necessary to clarify the effectiveness of tDCS and determine the optimal combination of tDCS parameters. [ABSTRACT FROM AUTHOR]

Exportin 1 (XPO1) is the major karyopherin‐β nuclear receptor mediating the nuclear export of hundreds of proteins and some classes of RNA and regulates several critical processes in the cell, including cell‐cycle progression, transcription and translation. Viruses have co‐opted XPO1 to promote nucleocytoplasmic transport of viral proteins and RNA. Maize mosaic virus (MMV) is a plant‐infecting rhabdovirus transmitted in a circulative propagative manner by the corn planthopper, Peregrinus maidis. MMV replicates in the nucleus of plant and insect hosts, and it remains unknown whether MMV co‐opts P. maidis XPO1 (PmXPO1) to complete its life cycle. Because XPO1 plays multiple regulatory roles in cell functions and virus infection, we hypothesized that RNAi‐mediated silencing of XPO1 would negatively affect MMV accumulation and insect physiology. Although PmXPO1 expression was not modulated during MMV infection, PmXPO1 knockdown negatively affected MMV accumulation in P. maidis at 12 and 15 days after microinjection. Likewise, PmXPO1 knockdown negatively affected P. maidis survival and reproduction. PmXPO1 exhibited tissue‐specific expression patterns with higher expression in the ovaries compared with the guts of adult females. Survival rate was significantly lower for PmXPO1 knockdown females, compared with controls, but no effect was observed for males. PmXPO1 knockdown experiments revealed a role for PmXPO1 in ovary function and egg production. Oviposition and egg hatch on plants were dramatically reduced in females treated with dsRNA PmXPO1. These results suggest that PmXPO1 is a positive regulator of P. maidis reproduction and that it plays a proviral role in the insect vector supporting MMV infection. [ABSTRACT FROM AUTHOR]

Background: Alcohol is commonly consumed by adolescents in a binge‐like pattern, which can lead to long‐lasting cognitive deficits, including reduced behavioral flexibility. We and others have determined that adolescent intermittent ethanol (AIE) exposure leads to increased number of perineuronal net (PNN) numbers in brain regions that are important for behavioral flexibility. However, whether altered neurochemistry stemming from AIE exposure plays a significant role in reduced behavioral flexibility is unknown. Methods: We measured the number and size of parvalbumin expressing (PV+) interneurons and associated PNNs within the orbitofrontal cortex (OFC), prelimbic cortex (PrL), infralimbic cortex (IL), and anterior insular cortex (AIC) of female and male rats following AIE or control exposure and subsequent training on an attentional set‐shift task (ASST). We then ran analyses to determine whether AIE‐induced changes in PV and PNN measures statistically mediated the AIE‐induced behavioral deficit in reversal learning. Results: We demonstrate that AIE exposure impaired behavioral flexibility on reversal two of the ASST (i.e., recalling the initial learned associations), and led to smaller PV+ cells and increased PNN numbers in the AIC. Interestingly, PNN size and number were not altered in the PrL or IL following AIE exposure, in contrast to prior reports. Mediation analyses suggest that AIE alters behavioral flexibility, at least in part through changes in PV and PNN fluorescent measures in the AIC. Conclusions: This study reveals a significant link between AIE exposure, neural alterations, and diminished behavioral flexibility in rats, and highlights a potential novel mechanism comprising changes in PV and PNN measures within the AIC. Future studies should explore the impact of PNN degradation within the AIC on behavioral flexibility. [ABSTRACT FROM AUTHOR]

Background: Although the World Health Organization recommends visible and clear warning labels about the risks of alcohol consumption on containers and advertising, many of the currently used labels are too small to be visible. This study investigated the brain activity (using fMRI) and alcohol consumption intentions of French young men exposed to two warning formats displayed on alcoholic beverage advertisements: a small Text‐only Alcohol Warning (TAW) currently used in many countries, and a larger text‐and‐picture alcohol warning (PAW). Methods: Seventy‐four eligible 18–25‐year‐old male drinkers completed a face‐to‐face individual visit with a physician expert in addiction medicine. This was followed by the fMRI session during which they viewed 288 stimuli [96 alcohol advertisements with TAWs, the same 96 advertisements with PAWs, and 96 water advertisements (controls)] for 3 s each. If the advertisement made participants want ("yes")/do not want ("no") to consume the product, they pressed the corresponding button (self‐report responses). The number of "yes" responses was compared between advertisement types with a paired sample t‐test. Whole‐brain and region‐of‐interest (ROI) analyses of the fMRI data were performed. Results: Whole‐brain BOLD fMRI highlighted contrasting effects of PAWs and TAWs. Compared with TAWs, PAWs elicited more activation in the precuneus, angular gyrus, occipital, frontal and temporal areas, and less activation in the nucleus accumbens, ventral tegmental areas, and putamen areas (regions of the reward circuit). The ROI analysis confirmed less activation in the reward circuit (left and right ventral tegmental areas, left and right nucleus accumbens) when viewing PAWs than TAWs. Analysis of the self‐report responses indicated that the desire to consume the advertised alcohol product was lower when PAWs were viewed (compared with TAWs) (T = 8.18, p < 10−11). Conclusions: This is the first fMRI study to assess the effect of different alcohol warning formats. Our findings show that compared with TAWs, stronger PAWs in advertisements elicited less activity in key regions of the reward system. This suggests that the effects may influence the desire to consume alcohol products (self‐report response analysis). These results could help policymakers who are interested in developing more effective labeling measures that target young people. [ABSTRACT FROM AUTHOR]

Objective: Binge‐eating disorder is an eating disorder characterized by recurrent binge‐eating episodes, during which individuals consume excessive amounts of highly palatable food (HPF) in a short time. This study investigates the intricate relationship between repeated binge‐eating episode and the transcriptional regulation of two key genes, adenosine A2A receptor (A2AAR) and dopamine D2 receptor (D2R), in selected brain regions of rats. Method: Binge‐like eating behavior on HPF was induced through the combination of food restrictions and frustration stress (15 min exposure to HPF without access to it) in female rats, compared to control rats subjected to only restriction or only stress or none of these two conditions. After chronic binge‐eating episodes, nucleic acids were extracted from different brain regions, and gene expression levels were assessed through real‐time quantitative PCR. The methylation pattern on genes' promoters was investigated using pyrosequencing. Results: The analysis revealed A2AAR upregulation in the amygdala and in the ventral tegmental area (VTA), and D2R downregulation in the nucleus accumbens in binge‐eating rats. Concurrently, site‐specific DNA methylation alterations at gene promoters were identified in the VTA for A2AAR and in the amygdala and caudate putamen for D2R. Discussion: The alterations on A2AAR and D2R genes regulation highlight the significance of epigenetic mechanisms in the etiology of binge‐eating behavior, and underscore the potential for targeted therapeutic interventions, to prevent the development of this maladaptive feeding behavior. These findings provide valuable insights for future research in the field of eating disorders. Public Significance: Using an animal model with face, construct, and predictive validity, in which cycles of food restriction and frustration stress evoke binge‐eating behavior, we highlight the significance of epigenetic mechanisms on adenosine A2A receptor (A2AAR) and dopamine D2 receptor (D2R) genes regulation. They could represent new potential targets for the pharmacological management of eating disorders characterized by this maladaptive feeding behavior. [ABSTRACT FROM AUTHOR]

We investigated the temporal impact of multisensory settings on children's learning of word‐object and action‐object associations at 1‐ and 2‐years of age. Specifically, we examined whether the temporal alignment of words and actions influenced the acquisition of novel word‐action‐object associations. We used a preferential looking and violation of expectation task in which infants and young children were first presented with two distinct word‐object and action‐object pairings either in a synchronous (overlapping in time) or sequential manner (one after the other). Findings revealed that 2‐year‐olds recognized both, action‐object and word‐object associations when they first saw the word‐action‐object combinations synchronously, but not sequentially, as evidenced by looking behavior. 1‐year‐olds did not show evidence for recognition for either of the word‐object and action‐object pairs, regardless of the initial temporal alignment of these cues. To control for individual differences, we explored factors that might influence associative learning based on parental reports of 1‐ and 2‐year‐olds development, however, developmental measures did not explain word‐action‐object associative learning in either group. We discuss that while young children may benefit from the temporal alignment of multisensory cues as it enables them to actively engage with the multisensory content in real‐time, infants may have been overwhelmed by the complexity of this input. [ABSTRACT FROM AUTHOR]

Background: Alcohol use disorder (AUD) is commonly associated with distressing psychological symptoms. Pathologic changes associated with AUD have been described in both the gut microbiome and brain, but the mechanisms underlying gut‐brain signaling in individuals with AUD are unknown. This study examined associations among the gut microbiome, brain morphometry, and clinical symptoms in treatment‐seeking individuals with AUD. Methods: We performed a secondary analysis of data collected during inpatient treatment for AUD in subjects who provided gut microbiome samples and had structural brain magnetic resonance imaging (MRI; n = 16). Shotgun metagenomics sequencing was performed, and the morphometry of brain regions of interest was calculated. Clinical symptom severity was quantified using validated instruments. Gut‐brain modules (GBMs) used to infer neuroactive signaling potential from the gut microbiome were generated in addition to microbiome features (e.g., alpha diversity and bacterial taxa abundance). Bivariate correlations were performed between MRI and clinical features, microbiome and clinical features, and MRI and microbiome features. Results: Amygdala volume was significantly associated with alpha diversity and the abundance of several bacteria including taxa classified to Blautia,Ruminococcus, Bacteroides, and Phocaeicola. There were moderate associations between amygdala volume and GBMs, including butyrate synthesis I, glutamate synthesis I, and GABA synthesis I & II, but these relationships were not significant after false discovery rate (FDR) correction. Other bacterial taxa with shared associations to MRI features and clinical symptoms included Escherichia coli and Prevotella copri. Conclusions: We identified gut microbiome features associated with MRI morphometry and AUD‐associated symptom severity. Given the small sample size and bivariate associations performed, these results require confirmation in larger samples and controls to provide meaningful clinical inferences. Nevertheless, these results will inform targeted future research on the role of the gut microbiome in gut‐brain communication and how signaling may be altered in patients with AUD. [ABSTRACT FROM AUTHOR]

Objectives: People with Alzheimer's Disease (AD) experience changes in their level and content of consciousness, but there is little research on biomarkers of consciousness in pre‐clinical AD and Mild Cognitive Impairment (MCI). This study investigated whether levels of consciousness are decreased in people with MCI. Methods: A multi‐site site magnetoencephalography (MEG) dataset, BIOFIND, comprising 83 people with MCI and 83 age matched controls, was analysed. Arousal (and drowsiness) was assessed by computing the theta‐alpha ratio (TAR). The Lempel‐Ziv algorithm (LZ) was used to quantify the information content of brain activity, with higher LZ values indicating greater complexity and potentially a higher level of consciousness. Results: LZ was lower in the MCI group versus controls, indicating a reduced level of consciousness in MCI. TAR was higher in the MCI group versus controls, indicating a reduced level of arousal (i.e. increased drowsiness) in MCI. LZ was also found to be correlated with mini‐mental state examination (MMSE) scores, suggesting an association between cognitive impairment and level of consciousness in people with MCI. Conclusions: A decline in consciousness and arousal can be seen in MCI. As cognitive impairment worsens, measured by MMSE scores, levels of consciousness and arousal decrease. These findings highlight how monitoring consciousness using biomarkers could help understand and manage impairments found at the preclinical stages of AD. Further research is needed to explore markers of consciousness between people who progress from MCI to dementia and those who do not, and in people with moderate and severe AD, to promote person‐centred care. Key points: Consciousness and Arousal in MCI: This study found that patients with Mild Cognitive Impairment (MCI) show reduced neural complexity and arousal levels, as measured by LZsum and theta‐alpha ratio (TAR), respectively. These reductions correlate with the severity of cognitive impairment.Correlation with Cognitive Tests: There is a significant correlation between the LZsum and TAR biomarkers and the Mini‐Mental State Examination (MMSE) scores, both overall and within the MCI group, indicating that these neural markers can reflect the extent of cognitive decline.Potential Early Indicators: The biomarkers used in the study not only showed a significant difference between MCI patients from controls, but are also sensitive to the degree of cognitive impairment, supporting their use in monitoring the early stages of dementia and suggesting that disruptions in consciousness may begin in preclinical stages.Implications for Management and Support: The findings underscore the importance of understanding subtle changes in arousal and awareness in MCI for patient‐cantered care. Such insights could help develop interventions to improve the daily functioning and quality of life of patients with MCI and Alzheimer's disease (AD), particularly as these changes in consciousness can affect decision‐making capacity, caregiver stress, and overall relationship quality. [ABSTRACT FROM AUTHOR]

Clinical trials of pharmacological candidates targeting the core features of autism have largely failed. This is despite evidence linking differences in multiple neurochemical systems to brain function in autism. While this has in part been explained by the heterogeneity of the autistic population, the field has largely relied upon association studies to link brain chemistry to function. The only way to directly establish that a neurotransmitter or neuromodulator is involved in a candidate brain function is to change it and observe a shift in that function. This experimental approach dominates preclinical neuroscience, but not human studies. There is little direct experimental evidence describing how neurochemical systems modulate information processing in the living human brain. Thus, our understanding of how neurochemical differences contribute to neurodiversity is limited, impeding our ability to translate findings from animal studies into humans. Here, we introduce our 'shiftability' paradigm, an approach to bridge the translational gap in autism research. We provide an overview of the guiding principles and methodologies we use to directly test the hypothesis that neurochemical systems function differently in autistic and non‐autistic individuals. [ABSTRACT FROM AUTHOR]

Background: Recent evidence suggests an elevated risk of cognitive impairment and dementia in individuals with atrial fibrillation (AF), irrespective of stroke occurrence. AF, known to reduce brain perfusion, particularly through silent cerebral ischemia, underscores the intricate relationship between cardiac and cerebral health. The heart plays a crucial role in supporting normal brain function, and rhythm control, a standard AF treatment, has demonstrated enhancements in brain perfusion. This systematic review aimed to examine published data concerning the influence of rhythm control on brain perfusion in patients with atrial fibrillation. Methods: A systematic search for relevant studies was carried out in Scopus, PubMed, Cochrane Reviews, ProQuest, and EBSCOhost, spanning from their inception until April 30, 2023. Studies that specifically examined brain perfusion following any form of rhythm control in atrial fibrillation were included in the review. Results: The review encompassed 10 studies involving 436 participants. Among these, six utilized electrical cardioversion for rhythm control. The majority (8 out of 10) demonstrated that restoring sinus rhythm markedly enhances brain perfusion. In one of the two remaining studies, notable improvement was observed specifically in a region closely linked to cognition. Additionally, both studies reporting data on the Mini-Mental State Examination (MMSE) showed a consistent and significant increase in scores following rhythm control. Conclusion: Successful rhythm control in AF emerges as a significant contributor to enhanced brain perfusion, suggesting a potential therapeutic avenue for reducing cognitive impairment incidence. However, further validation through larger prospective studies and randomized trials is warranted. [ABSTRACT FROM AUTHOR]

The article discusses the use of low-dose amitriptyline as a treatment for burning mouth syndrome (BMS), emphasizing its potential effectiveness based on a retrospective study. Topics discussed include the pharmacological action of amitriptyline in relation to serotonin and pain modulation, the neurological mechanisms involved in chronic pain and nociplastic pain, and the significance of brain network connectivity in managing pain associated with BMS.

Background: Executive function deficits (EFD) in late‐life depression (LLD) has been reported to be associated with antidepressant treatment resistance, increased disability, and poor quality of life. However, the underlying neutral mechanisms of EFD in patients with the first episode of LLD remains unclear. Methods: A total of 27 patients with first‐episode, drug‐naive LLD and 27 non‐depressed controls (NC) were recruited for the present research. Participants underwent the Trail Making Test, the 17‐item Hamilton depression rating scale (HAMD‐17) test, and task‐state functional magnetic resonance imaging scans under the neutral Stroop task. LLD patients' executive functions, depressive symptoms, and brain activity were examined again after 6 months of antidepressant treatment. Results: Of the 27 LLD patients, 16 cases completed 6‐month follow‐ups. Patients in the LLD baseline group spent more time on the Trail Making Test A test than those in the NC group (p < 0.05). In the presence of an incongruency between the word color and meaning, the accuracy rate of the neutral Stroop task in the LLD baseline group was lower, and the reaction time was greater than that in the NC group, with statistically significant difference (p < 0.05). The HAMD‐17 score in the LLD follow‐up group was significantly lower than that in the LLD baseline group (p < 0.05). More activated brain regions were present in the LLD baseline group than in the NC group when performing the neutral Stroop task. Compared with the LLD baseline group, abnormal activation of relevant brains in the cingulate‐prefrontal‐parietal network of LLD patients still existed in the LLD follow‐up group. Conclusions: LLD patients engaged more brain areas than the NC group while performing the neutral Stroop task. Abnormal activation of the cingulate‐prefrontal‐parietal network could be a contributing factor to EFD in LLD. Trial registration: ChiCTR, ChiCTR2100042370 (Date of registration: 21/01/2021). Limits: We didn't enroll enough first‐episode, LLD patients, the robustness of the findings need to be confirmed by large sample clinical trials. Key points: The findings of this study suggest that there is no significant correlation between the relief of depressive symptoms and the improvement of executive dysfunction in individuals with first‐episode, late‐life depression (LLD).Patients with first‐episode, LLD engaged more brain areas than the normal control group while performing the neutral Stroop task.Abnormal activation of the cingulate‐prefrontal‐parietal network could be a contributing factor to executive function deficits in LLD. [ABSTRACT FROM AUTHOR]

Objectives: There is enormous potential to improve brain health and reduce the risk of cognitive decline and dementia based on modifiable risk factors. The Lifestyle for Brain Health (LIBRA) index was developed to quantify modifiable dementia risk or room for brain health improvement. The objective of the study was to investigate the utility of the LIBRA index in relation to cognitive functioning in a midlife to early late‐life sample of New Zealanders. Methods: A subsample (n = 1001) of the longitudinal New Zealand Health, Work and Retirement (NZHWR) study completed face‐to‐face cognitive assessments using the 'Kiwi' Addenbrooke's Cognitive Examination—Revised (ACE‐R) in 2010 and again in 2012, in addition to completing biennial NZHWR surveys on socioeconomic, health and wellbeing aspects. The LIBRA index was calculated incorporating information on 8 out of 12 modifiable health and lifestyle factors for dementia. Unadjusted and adjusted regression models and mixed effects models were used to inspect associations of LIBRA with cognitive functioning, cognitive impairment, and cognitive decline. Results: The analytical sample (n = 881 [88.0%], after considering exclusion criteria and missing data) had a mean age of 63.1 (SD = 6.5) years, 53.3% were female, 26.2% were Māori, and 61.7% were highly educated. Higher LIBRA scores (indicating higher modifiable dementia risk) were associated with lower cognitive functioning (B = −0.33, 95% CI = −0.52;−0.15, p < 0.001) and a higher likelihood of cognitive impairment (OR = 1.22, 95% CI = 1.04; 1.42, p = 0.013), but did not predict cognitive decline over 2 years (B = −0.03, 95% CI = −0.22; 0.16, p = 0.766), adjusted for age, age2, gender, education, and ethnicity. Conclusions: The LIBRA index indicated promising utility for quantifying modifiable dementia risk in midlife and early late‐life New Zealanders. For local use, refinement of the LIBRA index should consider cultural differences in health and lifestyle risk factors, and further investigate its utility with a wider range of modifiable factors over a longer observation period. Key points: A higher Lifestyle for Brain Health (LIBRA) score was associated with lower cognitive functioning and a higher likelihood for cognitive impairment in midlife to early late‐life New ZealandersLIBRA can thus indicate room for improvement in brain health in New Zealanders aged 49–75 years oldFuture studies that investigate a broader range of modifiable risk factors for dementia might improve the utility of the LIBRA index [ABSTRACT FROM AUTHOR]

The overarching goal of this paper is to examine the efficacy of early intervention when viewed through the lens of developmental neuroscience. We begin by briefly summarizing neural development from conception through the first few postnatal years. We emphasize the role of experience during the postnatal period, and consistent with decades of research on critical periods, we argue that experience can represent both a period of opportunity and a period of vulnerability. Because plasticity is at the heart of early intervention, we next turn our attention to the efficacy of early intervention drawing from two distinct literatures: early intervention services for children growing up in disadvantaged environments, and children at elevated likelihood of developing a neurodevelopmental delay or disorder. In the case of the former, we single out interventions that target caregiving and in the case of the latter, we highlight recent work on autism. A consistent theme throughout our review is a discussion of how early intervention is embedded in the developing brain. We conclude our article by discussing the implications our review has for policy, and we then offer recommendations for future research. [ABSTRACT FROM AUTHOR]

Patients with severe traumatic brain injuries require urgent medical attention at a hospital. We evaluated whether transporting adult patients with a severe traumatic brain injury (TBI) to a Neuroscience Centre is associated with reduced mortality. We reviewed studies published between 2010 and 2023 on severe TBI in adults (>18 years) using Medline, CINAHL, Google Scholar and Cochrane databases. We focused on mortality rates and the impact of transferring patients to a Neuroscience Centre, delays to neurosurgery and EMS triage accuracy. This review analysed seven studies consisting of 53 365 patients. When patients were directly transported to a Neuroscience Centre, no improvement in survivability was demonstrated. Subsequently, transferring patients from a local hospital to a Neuroscience Centre was significantly associated with reduced mortality in one study (adjusted odds ratio: 0.79, 95% confidence interval: 0.64–0.96), and 24‐h (relative risk [RR]: 0.31, 0.11–0.83) and 30‐day (RR: 0.66, 0.46–0.96) mortality in another. Patients directly transported to a Neuroscience Centre were more unwell than those taken to a local hospital. Subsequent transfers increased time to CT scanning and neurosurgery in several studies, although these were not statistically significant. Additionally, EMS could accurately triage. None of the included studies demonstrated statistically significant findings indicating that direct transportation to a Neuroscience Centre increased survivability for patients with severe traumatic brain injuries. Subsequent transfers from a non‐Neuroscience Centre to a Neuroscience Centre reduced mortality rates at 24 h and 30 days. Further research is required to understand the differences between direct transport and subsequent transfers to Neuroscience Centres. [ABSTRACT FROM AUTHOR]

Objective: Few studies have focused on brain structure in atypical anorexia nervosa (atypical AN). This study investigates differences in gray matter volume (GMV) between females with anorexia nervosa (AN) and atypical AN, and healthy controls (HC). Method: Structural magnetic resonance imaging data were acquired for 37 AN, 23 atypical AN, and 41 HC female participants. Freesurfer was used to extract GMV, cortical thickness, and surface area for six brain lobes and associated cortical regions of interest (ROI). Primary analyses employed linear mixed‐effects models to compare group differences in lobar GMV, followed by secondary analyses on ROIs within significant lobes. We also explored relationships between cortical gray matter and both body mass index (BMI) and symptom severity. Results: Our primary analyses revealed significant lower GMV in frontal, temporal and parietal areas (FDR <.05) in AN and atypical AN when compared to HC. Lobar GMV comparisons were non‐significant between atypical AN and AN. The parietal lobe exhibited the greatest proportion of affected cortical ROIs in both AN versus HC and atypical AN versus HC. BMI, but not symptom severity, was found to be associated with cortical GMV in the parietal, frontal, temporal, and cingulate lobes. No significant differences were observed in cortical thickness or surface area. Discussion: We observed lower GMV in frontal, temporal, and parietal areas, when compared to HC, but no differences between AN and atypical AN. This indicates potentially overlapping structural phenotypes between these disorders and evidence of brain changes among those who are not below the clinical underweight threshold. Public significance: Despite individuals with atypical anorexia nervosa presenting above the clinical weight threshold, lower cortical gray matter volume was observed in partial, temporal, and frontal cortices, compared to healthy individuals. No significant differences were found in cortical gray matter volume between anorexia nervosa and atypical anorexia nervosa. This underscores the importance of continuing to assess and target weight gain in clinical care, even for those who are presenting above the low‐weight clinical criteria. [ABSTRACT FROM AUTHOR]

Regular participation in sports results in a series of physiological adaptations. However, little is known about the brain adaptations to physical activity. Here we aimed to investigate whether young endurance athletes and non‐athletes differ in the gray and white matter of the brain and whether cardiorespiratory fitness (CRF) is associated with these differences. We assessed the CRF, volumes of the gray and white matter of the brain using structural magnetic resonance imaging (sMRI), and brain white matter connections using diffusion magnetic resonance imaging (dMRI) in 20 young male endurance athletes and 21 healthy non‐athletes. While total brain volume was similar in both groups, the white matter volume was larger and the gray matter volume was smaller in the athletes compared to non‐athletes. The reduction of gray matter was located in the association areas of the brain that are specialized in processing of sensory stimuli. In the microstructure analysis, significant group differences were found only in the association tracts, for example, the inferior occipito‐frontal fascicle (IOFF) showing higher fractional anisotropy and lower radial diffusivity, indicating stronger myelination in this tract. Additionally, gray and white matter brain volumes, as well as association tracts correlated with CRF. No changes were observed in other brain areas or tracts. In summary, the brain signature of the endurance athlete is characterized by changes in the integration of sensory and motor information in the association areas. This study unveils the intriguing relationship between regular endurance sports participation, brain structure, and cardiorespiratory fitness. The findings shed light on the intricate interplay between physical activity and brain physiology, contributing valuable insights to our understanding of the brain's response to exercise. [ABSTRACT FROM AUTHOR]

The contemporary visibility of 'digital addictions' to online gaming, watching pornography, social media and so on suggests the discovery of some new form of technologically facilitated disease. Yet, what we actually see in the symptoms of these various behaviours when described as 'addictions' are a series of social problems that range from the interpersonal to the sociocultural. In the current article, I work to step outside of the individualising tendency of an addiction taxonomy to instead view digital addictions as a process of social diagnosis. In this way, digital addictions are understood as a reaction to historically and socioculturally informed forces. Specifically, I contend that a social diagnosis of the digital addiction concept tells us a great deal about contemporary cultural anxiety towards the ubiquity of digital media in our social worlds as it rubs up against concerns for productivity, socially lauded ideas of ostensibly 'natural' behaviours and worries about self‐governance and self‐control. I conclude with a series of pertinent questions about digital technologies, which are elided—if not actively foreclosed—within an addiction framework and which can better be made sense of by understanding digital addictions as a process of social diagnosis rather than the expression of a new kind of Internet borne illness. [ABSTRACT FROM AUTHOR]

Background: Childhood maltreatment is one of the most important preventable risk factors for a wide variety of psychiatric disorders. Further, when psychiatric disorders emerge in maltreated individuals they typically do so at younger ages, with greater severity, more psychiatric comorbid conditions, and poorer response to established treatments, resulting in a more pernicious course with an increased risk for suicide. Practitioners treating children, adolescents, and young adults with psychiatric disorders will likely encounter the highest prevalence of clients with early‐onset maltreatment‐associated psychiatric disorders. These may be some of their most challenging cases. Method: In this report, we explore key validated alterations in brain structure, function, and connectivity associated with exposure to childhood maltreatment as potential mechanisms behind their patients' clinical presentations. Results: We then summarize key behavioral presentations likely associated with neurobiological alterations and propose a toolkit of established trauma and skills‐based strategies that may help diminish symptoms and foster recovery. We also discuss how some of these alterations may serve as latent vulnerability factors for the possible development of future psychopathology. Conclusions: Research on the neurobiological consequences of childhood adversity provides a vastly enriched biopsychosocial understanding of the developmental origins of health and pathology that will hopefully lead to fundamental advances in clinical psychology and psychiatry. [ABSTRACT FROM AUTHOR]

Given the detrimental effects of excessive reactive oxygen species (ROS) accumulation in plant cells, various antioxidant mechanisms have evolved to maintain cellular redox homeostasis, encompassing both enzymatic components (e.g., catalase, superoxide dismutase) and non‐enzymatic ones. Despite extensive research on the role of antioxidant systems in plant physiology and responses to abiotic stresses, the potential exploitation of antioxidant enzymes by plant viruses to facilitate viral infection remains insufficiently addressed. Herein, we demonstrate that maize catalases (ZmCATs) exhibited up‐regulated enzymatic activities upon sugarcane mosaic virus (SCMV) infection. ZmCATs played crucial roles in SCMV multiplication and infection by catalysing the decomposition of excess cellular H2O2 and promoting the accumulation of viral replication‐related cylindrical inclusion (CI) protein through interaction. Peroxisome‐localized ZmCATs were found to be distributed around SCMV replication vesicles in Nicotiana benthamiana leaves. Additionally, the helper component‐protease (HC‐Pro) of SCMV interacted with ZmCATs and enhanced catalase activities to promote viral accumulation. This study unveils a significant involvement of maize catalases in modulating SCMV multiplication and infection through interaction with two viral factors, thereby enhancing our understanding regarding viral strategies for manipulating host antioxidant mechanisms towards robust viral accumulation. [ABSTRACT FROM AUTHOR]

Background: People with an acquired brain injury (ABI) find it challenging to use social media due to changes in their cognition and communication skills. Using social media can provide opportunities for positive connection, but there is a lack of interventions specifically designed to support safe and successful social media use after ABI. Aims: To investigate the outcomes of completing a social media skills intervention and identify barriers and facilitators for future implementation. Methods & Procedures: The study used a mixed‐methods, pre‐post‐intervention design. A total of 17 adults with an ABI were recruited. Participants completed an intervention that included a short self‐guided course about social media skills (social‐ABI‐lity course), and then participated in a private, moderated Facebook group over a 12‐week period (social‐ABI‐lity Facebook group). Data were collected over this period through observation of group activity and weekly surveys. They were also collected on social media use and quality of life at pre‐intervention, post‐intervention and after 3 months. Participants provided feedback on the experience of participating in the programme via a post‐intervention interview. Outcomes & Results: At post‐intervention, there were significant improvements in confidence in using Facebook (p = 0.002) and enjoyment of using Facebook to connect with others (p = 0.013). There was no significant change in reported quality of life, although participants described the multiple benefits of connection they perceived from involvement in the group. Observational data and feedback interviews were informative about the feasibility and acceptability of the intervention. Conclusions & Implications: This pilot study provided preliminary evidence that an intervention comprising a short, self‐guided training course and a private, moderated Facebook group improved outcomes for people with ABI. Key recommendations for future implementation include embedding active peer moderators within groups and taking an individualized approach to delivery of the intervention. WHAT THIS PAPER ADDS: What is already known on the subject: Research has documented the challenges that people with ABI experience in using social media, and the difficulty for rehabilitation clinicians in providing appropriate support in this field. What this paper adds to existing knowledge: This pilot study reports the outcomes of people with ABI completing a short, self‐guided social media skills course and participating in a private, moderated Facebook group. After the intervention, participants reported significantly increased confidence and enjoyment in using Facebook, described the benefits of connection found in the groups, and suggested potential improvements for future implementation. What are the potential or actual clinical implications of this work?: With the growing use of social media for connection and participation, there is a professional obligation to address social media communication skills in cognitive–communication rehabilitation for people with ABI. The findings of this study will inform interventions and future research to assist people with ABI to build their social media skills for communication, social support and a sense of connection. [ABSTRACT FROM AUTHOR]

Aim: To investigate the alterations of functional brain activity and connectivity in female nurses working on long‐term shifts and explore their correlations with work‐related psychological traits. Design: An exploratory cross‐sectional study. Methods: Thirty‐five female nurses working on long‐term shifts (shift nurses) and 35 female nurses working on fixed days (fixed nurses) were enrolled. After assessing the work‐related psychological traits, including burnout, perceived stress, anxiety, and depression of nurses, the fractional amplitude of low‐frequency fluctuations (fALFF) and region of interest (ROI)‐based functional connectivity (FC) analyses were performed to investigate the differences of brain spontaneous activity and functional connectivity between these two groups of nurses. Thereafter, correlations between the functional brain parameters (fALFF and FC) and clinical metrics were investigated among the shift nurses. Results: Compared to fixed nurses, shift nurses had higher burnout, perceived stress and depression scores, lower fALFF in the right dorsolateral prefrontal cortex (dlPFC), left and right superior parietal lobule (SPL), bilateral anterior cingulate cortex (ACC), and higher fALFF in the right superior/middle temporal gyrus, as well as decreased FC between the right dlPFC (the selected ROI) and bilateral ACC, left and right inferior frontal/orbitofrontal gyrus (IFG/IOFG), right SPL, and left middle occipital gyrus (voxel‐level p < 0.001, cluster level p < 0.05, GRF correction). Correlation analyses demonstrated that the fALFF value of the right dlPFC was significantly correlated with the burnout and anxiety scores, the FC value of the right dlPFC‐right SPL was correlated with the perceived stress and burnout scores, the FC value of the right dlPFC‐right IFG/IOFG was correlated with the burnout score in shift nurses (p < 0.05). Conclusion: Shift nurses had work‐related altered functional activity and connectivity in the right frontoparietal network, which provided objective and visualised evidence to clarify the hazards of long‐term shift work on female nurses. Patient or Public Contribution: Seventy nurses participated deeply as subjects in this study. These findings are expected to draw managers' attention to the harmful influences of shift work on nurses. [ABSTRACT FROM AUTHOR]

Aim: The present study aimed to examine whether dietary diversity is associated with cognitive impairment, including mild cognitive impairment (MCI), in community‐dwelling older Japanese adults. Methods: This cross‐sectional study was carried out in a general community setting. MCI and global cognitive impairment (GCI) were assessed using the Mini‐Mental State Examination and National Center for Geriatrics and Gerontology‐Functional Assessment Tool, which are multicomponent neurocognitive tests that include memory attention, executive function and processing speed. Dietary diversity was assessed using the diet variety score. The diet variety score assessed the 1‐week consumption frequency of 10 food groups, and either 0 or 1 point was allocated to each category based on the following responses: (i) "eat almost every day" (1 point); and (ii) "not eaten almost daily" (0 points). Older adults with a diet variety score of ≥3 points were defined as having high dietary diversity. Results: Data included 8987 older adults (mean age 73.9 ± 5.5 years; men 44.3%). The overall prevalences of MCI and GCI were 17.1% (n = 1538) and 8.4% (n = 753), respectively. The proportion of patients with a high dietary diversity was 69.9% (n = 6286). Multinomial logistic regression analysis revealed high dietary diversity was associated with MCI (OR 0.83, 95% CI 0.73–0.94) and GCI (OR 0.77, 95% CI 0.65–0.92) after adjusting for covariates. Conclusions: This study had a large sample size of older Japanese adults, and showed that high dietary diversity was associated with a lower proportion of MCI and GCI among older adults. Geriatr Gerontol Int 2024; 24: 75–81. [ABSTRACT FROM AUTHOR]

Aims: Vulnerable older adults tend to decrease physical activity (PA) and increase sedentary time (ST). Previous research on the associations between ST and brain volume have yielded inconsistent findings, without considering the impact of cognitive engagement (CE) on cognitive function. We aimed to examine the association between ST with CE and brain volume. Methods: A structural magnetic resonance imaging survey was conducted among community‐dwelling vulnerable older adults. Brain volumetric measurements were obtained using 3T magnetic resonance imaging and pre‐processed using FreeSurfer. ST with low or high CE was assessed using a 12‐item questionnaire. PA was assessed by the frequency of light and moderate levels of physical exercise according to the Japanese version of the Cardiovascular Health Study criteria. Participants were categorized into a low PA group and a moderate‐to‐high PA group. Results: Among 91 participants (83.1 ± 5.2 years old, 61.5% female), 26 were low PA. The overall sample and moderate‐to‐high PA group did not show significant positive associations with brain volume for ST with high CE. In the low PA group, isotemporal substitution models showed that replacing ST with low CE by ST with high CE was significantly associated with increased brain volume in some areas, including the rostral and caudal anterior cingulate (β = 0.486–0.618, all P < 0.05, adjusted R2 = 0.344–0.663). Conclusions: Our findings suggest that replacing ST with low CE by ST with high CE is positively associated with brain volume in vulnerable older adults with low PA. Geriatr Gerontol Int 2024; 24: 82–89. [ABSTRACT FROM AUTHOR]

Objective: Fibromyalgia (FM) is characterized by pervasive pain‐related symptomatology and high levels of negative affect. Mind–body treatments such as cognitive behavioral therapy (CBT) appear to foster improvement in FM via reductions in pain‐related catastrophizing, a set of negative, pain‐amplifying cognitive and emotional processes. However, the neural underpinnings of CBT's catastrophizing‐reducing effects remain uncertain. This randomized controlled mechanistic trial was designed to assess CBT's effects on pain catastrophizing and its underlying brain circuitry. Methods: Of 114 enrolled participants, 98 underwent a baseline neuroimaging assessment and were randomized to 8 weeks of individual CBT or a matched FM education control (EDU) condition. Results: Compared with EDU, CBT produced larger decreases in pain catastrophizing post treatment (P < 0.05) and larger reductions in pain interference and symptom impact. Decreases in pain catastrophizing played a significant role in mediating those functional improvements in the CBT group. At baseline, brain functional connectivity between the ventral posterior cingulate cortex (vPCC), a key node of the default mode network (DMN), and somatomotor and salience network regions was increased during catastrophizing thoughts. Following CBT, vPCC connectivity to somatomotor and salience network areas was reduced. Conclusion: Our results suggest clinically important and CBT‐specific associations between somatosensory/motor‐ and salience‐processing brain regions and the DMN in chronic pain. These patterns of connectivity may contribute to individual differences (and treatment‐related changes) in somatic self‐awareness. CBT appears to provide clinical benefits at least partially by reducing pain‐related catastrophizing and producing adaptive alterations in DMN functional connectivity. [ABSTRACT FROM AUTHOR]

Purpose: To compare the strength of associations between different indices of cardiorespiratory fitness (CRF) and brain health outcomes in children with overweight/obesity. Methods: Participants were 100 children aged 8–11 years. CRF was assessed using treadmill exercise test (peak oxygen uptake [V̇O2peak], treadmill time, and V̇O2 at ventilatory threshold) and 20‐metre shuttle run test (20mSRT, laps, running speed, estimated V̇O2peak using the equations by Léger et al., Mahar et al., and Matsuzaka et al.). Intelligence, executive functions, and academic performance were assessed using validated methods. Total gray matter and hippocampal volumes were assessed using structural MRI. Results: V̇O2peak/body mass (β = 0.18, 95% CI = 0.01–0.35) and treadmill time (β = 0.18–0.21, 95% CI = 0.01–0.39) were positively associated with gray matter volume. 20mSRT laps were positively associated with executive functions (β = 0.255, 95% CI = 0.089–0.421) and academic performance (β = 0.199–0.255, 95% CI = 0.006–0.421), and the running speed was positively associated with executive functions (β = 0.203, 95% CI = 0.039–0.367). Estimated V̇O2peak/Léger et al. was positively associated with intelligence, executive functions, academic performance, and gray matter volume (β = 0.205–0.282, 95% CI = 0.013–0.500). Estimated V̇O2peak/Mahar et al. and V̇O2peak/Matsuzaka et al. (speed) were positively associated with executive functions (β = 0.204–0.256, 95% CI = 0.031–0.436). Conclusion: Although V̇O2peak is considered the gold standard indicator of CRF in children, peak performance (laps or running speed) and estimated V̇O2peak/Léger et al. derived from 20mSRT had stronger and more consistent associations with brain health outcomes than other indices of CRF in children with overweight/obesity. [ABSTRACT FROM AUTHOR]

Studies have shown that neural responses following concentric (CON) and eccentric (ECC) muscle contractions are different, which suggests differences in motor control associated with CON and ECC contractions. This study aims to determine brain activation of the left primary motor cortex (M1) and left and right dorsolateral prefrontal cortices (DLPFCs) during ECC and CON of the right bicep brachii (BB) muscle at low‐ and high‐contraction intensities. Eighteen young adults (13M/5F, 21–35 years) were recruited to participate in one familiarization and two testing sessions in a randomized crossover design. During each testing session, participants performed either ECC or CON contractions of the BB (3 sets × 8 reps) at low‐ (25% of maximum ECC/CON, 45°/s) and high‐intensity (75% of maximum ECC/CON, 45°/s) on an isokinetic dynamometer. Eleven‐channel functional near‐infrared spectroscopy was used to measure changes in oxyhemoglobin (O2Hb) from the left M1, and left and right DLPFC during ECC and CON contractions. Maximum torque for ECC was higher than CON (43.3 ± 14.1 vs. 46.2 ± 15.7 N m, p = 0.025); however, no differences in O2Hb were observed between contraction types at low or high intensities in measured brain regions. High‐intensity ECC and CON contractions resulted in greater increases in O2Hb of M1 and bilateral DLPFC compared to low‐intensity ECC and CON contractions (p = 0.014). Our findings suggest no differences in O2Hb responses between contraction types at high and low intensities. High‐contraction intensities resulted in greater brain activation of the M1 and bilateral DLPFC, which may have implications for neurorehabilitation to increase central adaptations from exercise. [ABSTRACT FROM AUTHOR]

We argue that in implanted neurotechnology research, participants and researchers experience what Henry Richardson has called "moral entanglement." Participants partially entrust researchers with access to their brains and thus to information that would otherwise be private, leading to created intimacies and special obligations of beneficence for researchers and research funding agencies. One of these obligations, we argue, is about continued access to beneficial technology once a trial ends. We make the case for moral entanglement in this context through exploration of participants' vulnerability, uncompensated risks and burdens, depth of relationship with the research team, and dependence on researchers in implanted neurotechnology trials. [ABSTRACT FROM AUTHOR]

Inequities with regard to brain health, economic costs, and the evidence base for dementia care continue. Achieving health equity in dementia care requires rigorous efforts that ensure disproportionately affected populations participate fully in—and benefit from—clinical research. Embedding‐proven interventions under real‐world conditions and within existing healthcare systems have the potential to examine the effectiveness of an intervention, improve dementia care, and leverage the use of existing resources. Developing embedded pragmatic controlled trials (ePCT) research designs for nonpharmacological dementia care interventions involves a plethora of a priori assumptions and decisions. Although frameworks exist to determine whether interventions are "ready" for ePCT, there is no heuristic to assess health equity‐readiness. We discuss health equity considerations, case examples, and research strategies across ePCT study domains of evidence, risk, and alignment. Future discussions regarding health equity considerations across other domains are needed. [ABSTRACT FROM AUTHOR]

Monoaminergic systems are conserved in vertebrates, yet they present variations in neuroanatomy, genetic components and functions across species. MonoAmine Oxidase, or MAO, is the enzyme responsible for monoamine degradation. While mammals possess two genes, MAO‐A and MAO‐B, fish possess one single mao gene. To study the function of MAO and monoamine homeostasis on fish brain development and physiology, here we have generated a mao knockout line in Astyanax mexicanus (surface fish), by CRISPR/Cas9 technology. Homozygote mao knockout larvae died at 13 days post‐fertilization. Through a time‐course analysis, we report that hypothalamic serotonergic neurons undergo fine and dynamic regulation of serotonin level upon loss of mao function, in contrast to those in the raphe, which showed continuously increased serotonin levels – as expected. Dopaminergic neurons were not affected by mao loss‐of‐function. At behavioral level, knockout fry showed a transient decrease in locomotion that followed the variations in the hypothalamus serotonin neuronal levels. Finally, we discovered a drastic effect of mao knockout on brain progenitors proliferation in the telencephalon and hypothalamus, including a reduction in the number of proliferative cells and an increase of the cell cycle length. Altogether, our results show that MAO has multiple and varied effects on Astyanax mexicanus brain development. Mostly, they bring novel support to the idea that serotonergic neurons in the hypothalamus and raphe of the fish brain are different in nature and identity, and they unravel a link between monoaminergic homeostasis and brain growth. [ABSTRACT FROM AUTHOR]

Introduction: To investigate changes in the multilayer network in patients with migraine compared to healthy controls. Methods: This study enrolled 82 patients with newly diagnosed migraine without aura and 53 healthy controls. Brain magnetic resonance imaging (MRI) was conducted using a 3‐tesla MRI scanner, including three‐dimensional T1‐weighted and diffusion tensor imaging (DTI). A gray matter layer matrix was created with a morphometric similarity network using T1‐weighted imaging and the FreeSurfer program. A white matter layer matrix was also created with structural connectivity using the DTI studio (DSI) program. A multilayer network analysis was then performed by applying graph theory using the BRAPH program. Results: Significant changes were observed in the multilayer network at the global level in patients with migraines compared to the healthy controls. The multilayer modularity (0.177 vs. 0.160, p =.0005) and average multiplex participation (0.934 vs. 0.924, p =.002) were higher in patients with migraines than in the healthy controls. In contrast, the average multilayer clustering coefficient (0.406 vs. 0.461, p =.0005), average overlapping strength (56.061 vs. 61.676, p =.0005), and average weighted multiplex participation (0.847 vs. 0.878, p =.0005) were lower in patients with migraine than in the healthy controls. In addition, several regions showed significant changes in the multilayer network at the nodal level, including multiplex participation, multilayer clustering coefficients, overlapping strengths, and weighted multiplex participation. Conclusion: This study demonstrated significant changes in the multilayer network in patients with migraines compared to healthy controls. This could aid an understanding of the complex brain network in patients with migraine and may be associated with the pathophysiology of migraines. Patients with migraine show multilayer network changes in widespreading brain regions compared to healthy controls, and specific brain areas seem to play a hub role for pathophysiology of the migraine. [ABSTRACT FROM AUTHOR]

It has long been recognized that an individual's experiences can metaphorically 'get under the skin' and become biologically embedded, thus affecting behavior and life outcomes (Hertzman, 2012). While this term is most often used to describe how adverse experiences influence biological process, it is rarely discussed how the same can be said of positive experiences, such as intervention to prevent or treat negative outcomes. In their annual review, Nelson et al. (2023) provide a timely and comprehensive review of how early intervention capitalizes on the neuroplasticity of the postnatal years, turning periods of 'vulnerability' to ones of 'opportunity'. Drawing on decades of expertise, they discuss the neurobiological mechanisms of intervention in two contexts: caregiving interventions for children growing up in disadvantaged environments, and therapeutic interventions for children at elevated risk of neurodevelopmental disorders such as Autism. They thought‐provokingly describe both how early intervention operates through mechanisms of neural plasticity and how this can and should inform policy decisions to provide the greatest benefit to children. Here, I aim to underscore the importance of this review by addressing the intersection of these topics; specifically, I muse on how the scientific discovery of biological processes and the ethical imperative to support vulnerable children's development are intimately intertwined, and how this highlights both critical lines of future inquiry as well as policy implications. [ABSTRACT FROM AUTHOR]

Background: Adolescence, a developmental period characterized by significant changes in sleep, is associated with normative increases in impulsivity. While short sleep duration has been linked to elevated impulsivity, the neural mechanism underlying the relationship between short sleep duration and elevated impulsivity remains poorly understood. Methods: We analyzed a dataset of 7,884 drug‐naive 9–10 year‐olds from the Adolescent Brain Cognitive Development (ABCD) study. Among them, 5,166 have two‐year follow‐up neuroimaging data. Linear mixed‐effects models, mediation analyses, and longitudinal mediation analyses were used to investigate the relationship between parent‐reported sleep duration, impulsivity, and functional and structural connectivity between the cortex and the striatum. Results: We found that less sleep duration is significantly associated with higher positive and negative urgency, which are two affect‐related components of impulsivity. In addition, we observed a link between short sleep duration and reduced corticostriatal connectivity. Neural pathways associated with short sleep duration—functional connectivity between the cingulo‐opercular network and the left caudate, and between the cingulo‐parietal network and the right pallidum—mediated the association between sleep duration and positive urgency both at baseline and two‐year follow‐up. Longitudinal mediation analyses further revealed that short sleep duration and elevated positive urgency exacerbated each other through these two corticostriatal connectivities. Conclusions: These findings highlight the key role of corticostriatal connectivities in the reciprocal relationship between short sleep duration and elevated impulsivity. Given the increasing prevalence of short sleep duration in adolescents, the link between sleep duration, impulsivity, and corticostriatal connectivities has important implications for timely interventions to address impulsive problems in early adolescents. [ABSTRACT FROM AUTHOR]

Background: Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by difficulties in social communication and interaction. Crucial for efficient social interaction is the ability to quickly and accurately extract information from a person's face. Frequency‐tagging electroencephalography (EEG) is a novel tool to quantify face‐processing sensitivity in a robust and implicit manner. In terms of intervention approaches, intranasal administration of oxytocin (OT) is increasingly considered as a potential pharmacological approach for improving socio‐communicative difficulties in ASD, through enhancing social salience and/or reducing (social) stress and anxiety. Methods: In this randomized, double‐blind, placebo‐controlled, mechanistic pharmaco‐neuroimaging clinical trial, we implemented frequency‐tagging EEG to conduct an exploratory investigation into the impact of repeated OT administration (4 weeks, 12 IU, twice daily) on neural sensitivity towards happy and fearful facial expressions in children with ASD (8–12 years old; OT: n = 29; placebo: n = 32). Neural effects were assessed at baseline, post‐nasal spray (24 hr after the last nasal spray) and at a follow‐up session, 4 weeks after the OT administration period. At baseline, neural assessments of children with ASD were compared with those of an age‐ and gender‐matched cohort of neurotypical (NT) children (n = 39). Results: Children with ASD demonstrated reduced neural sensitivity towards expressive faces, as compared to NT children. Upon nasal spray administration, children with ASD displayed a significant increase in neural sensitivity at the post‐ and follow‐up sessions, but only in the placebo group, likely reflecting an implicit learning effect. Strikingly, in the OT group, neural sensitivity remained unaffected from the baseline to the post‐session, likely reflecting a dampening of an otherwise typically occurring implicit learning effect. Conclusions: First, we validated the robustness of the frequency‐tagging EEG approach to assess reduced neural sensitivity towards expressive faces in children with ASD. Furthermore, in contrast to social salience effects observed after single‐dose administrations, repeated OT administration dampened typically occurring learning effects in neural sensitivity. In line with OT's social anxiolytic account, these observations possibly reflect a predominant (social) stress regulatory effect towards emotionally evocative faces after repeated OT administration. [ABSTRACT FROM AUTHOR]

Background: Parkinson's disease (PD) is the second most common progressive neurodegenerative disorder. Exercise protocols are promising interventions to improve PD symptoms, however, the best modality and its neural correlates are still unknown. Objectives: To evaluate the effects of the aerobic, strength and task‐oriented upper‐limb exercises in motor function, manual dexterity, and brain oscillations of individuals with PD. Method: In this clinical trial, 44 PD patients aged 40–80 years will be randomized in four groups: aerobic training (AT), strength training (ST), task‐oriented training (TOT), and waiting list group (CG). The AT group will perform 30 min of a cycle ergometer on 50%–70% of the reserve heart rate. The ST group will use equipment for upper limb muscles and will perform two series of 8–12 repetitions for each exercise, and intensity between 50% and 70% of one maximum repetition will be used. The TOT group will perform a program consisting of three activities to enhance reaching, grasping, and manipulation. All the groups will perform three sessions per week for 8 weeks. We will use the UPDRS Motor function section, Nine‐Hole Peg Test, and quantitative electroencephalography to measure motor function, manual dexterity, and brain oscillations, respectively. ANOVA and regression models will be used to compare outcomes within and between groups. [ABSTRACT FROM AUTHOR]

We aimed to analyze the effect of a head‐to‐head virtual race on 20‐km time trial performance in well‐trained mentally fatigued cyclists. A total of 24 male professional cyclists participated in the present study, which was conducted in a within‐factors design [four experimental conditions × four times (throughout 20‐km time trial cycling)]. An avatar representing the participant on the racecourse was visible during the time trials. Then, a second virtual avatar representing the opponent was projected onto the screen in the mental fatigue head‐to‐head and control head‐to‐head experimental conditions. Measurements [rating of perceived exertion, heart rate, and eye‐tracking measures (i.e., pupil diameter)] were performed every 5‐km throughout the 20‐km time trial. As a result, impaired total time, power output, and cadence throughout the 20‐km cycling time trial were found for mental fatigue compared to mental fatigue head‐to‐head, control head‐to‐head, and control conditions (p < 0.05). Also, impaired 20‐km time trial performance (total time, power output, and cadence) was found for mental fatigue head‐to‐head compared to control head‐to‐head (p < 0.05). Moreover, lower RPE was found for the control and control head‐to‐head conditions than mental fatigue head‐to‐head and mental fatigue experimental conditions (p < 0.05). Higher pupil diameter was also found for mental fatigue head‐to‐head, control head‐to‐head, and control than the mental fatigue experimental condition (p < 0.05). In summary, the overall performance throughout the 20‐km cycling time trial was improved by the presence of a virtual opponent for the mentally fatigued cyclists. [ABSTRACT FROM AUTHOR]

Objectives: Mastication is associated with brain activation at the primary somatosensory cortex (S1) and the primary motor cortex (M1). Masticatory functions differ between patients with cognitive impairment (CI) and cognitively healthy older adults (non‐CI). The association between cognitive health, brain network of functional connectivity, and mastication has remained unknown. The study investigated the association between masticatory performance (MP) and the topological feature of the functional network at the M1 and S1 in the CI and non‐CI groups. Subjects and Methods: Forty‐nine non‐CI and 15 CI subjects received resting‐state (rs) fMRI and assessment of MP. The topological feature of the M1 and S1 was quantified by eigenvector centrality (EC), an index that reflects a brain region as a functional "hub" of brain network. Results: In the non‐CI group, MP was significantly correlated with EC of the left M1 and the right M1. The correlation was not statistically significant in the CI group. Cognitive status (CI or non‐CI) and EC of the left M1 and the right M1, respectively, were statistically significant predictors to individual MP. Conclusion: Cognitive status and the topological feature of the M1 in the intrinsic functional network may contribute to the individual difference in masticatory function. [ABSTRACT FROM AUTHOR]

Trust is widely regarded as being foundational in workplace relationships. The violation of interpersonal trust results in a range of negative affective, cognitive and behavioural consequences for the injured party. However, research has yet to isolate the specific neural areas and processes activated when different types of interpersonal trust are breached. Using electroencephalogram with 68 participants, we identified the effects of three distinct types of trust violations—ability violation, integrity violation and benevolence violations—on electrical brain activity. Our findings indicate that trust violations are processed in social cognitive‐related brain areas. Specifically, our results identify the significance of the default mode network (DMN), relevant to the processing of social information, in trust violation and further isolated distinct activity for ability, integrity and benevolence trust violation, with integrity violations demonstrating the greatest reaction in the DMN. Benevolence violations generated the next greatest reaction but were not significantly different from the ability violations. This potential distinction may be worth further investigation in future research. Our findings highlight the potential importance of the DMN in processing cues regarding the trustworthiness of others and the distinctiveness of the processing of violation cues of the three facets of trustworthiness. [ABSTRACT FROM AUTHOR]

DNA damage is a central contributor to the aging process. In the brain, a major threat to the DNA is the considerable amount of reactive oxygen species produced, which can inflict oxidative DNA damage. This type of damage is removed by the base excision repair (BER) pathway, an essential DNA repair mechanism, which contributes to genome stability in the brain. Despite the crucial role of the BER pathway, insights into how this pathway is affected by aging in the human brain and the underlying regulatory mechanisms are very limited. By microarray analysis of four cortical brain regions from humans aged 20–99 years (n = 57), we show that the expression of core BER genes is largely downregulated during aging across brain regions. Moreover, we find that expression of many BER genes correlates positively with the expression of the neurotrophin brain‐derived neurotrophic factor (BDNF) in the human brain. In line with this, we identify binding sites for the BDNF‐activated transcription factor, cyclic‐AMP response element‐binding protein (CREB), in the promoter of most BER genes and confirm the ability of BDNF to regulate several BER genes by BDNF treatment of mouse primary hippocampal neurons. Together, these findings uncover the transcriptional landscape of BER genes during aging of the brain and suggest BDNF as an important regulator of BER in the human brain. [ABSTRACT FROM AUTHOR]

Background: Exercise for people with whiplash associated disorder (WAD) induces hypoalgesic effects in some, but hyperalgesic effects in others. We investigated the exercise‐induced neurobiological effects of aerobic and strengthening exercise in individuals with chronic WAD. Methods: Sixteen participants (8 WAD, 8 pain‐free [CON]) were randomised to either aerobic or strengthening exercise. MRI for brain morphometry, functional MRI for brain connectivity, and magnetic resonance spectroscopy for brain biochemistry, were used at baseline and after the 8‐week intervention. Results: There were no differences in brain changes between exercise groups in either the WAD or CON group, therefore aerobic and strengthening data were combined to optimise sample size. After the exercise intervention, the CON group demonstrated increased cortical thickness (left parahippocampus: mean difference = 0.04, 95% CI = 0.07–0.00, p = 0.032; and left lateral orbital frontal cortex: mean difference = 0.03, 95% CI = 0.00–0.06, p = 0.048). The WAD group demonstrated an increase in prefrontal cortex (right medial orbital frontal) volume (mean difference = 95.57, 95% CI = 2.30–192.84, p = 0.046). Functional changes from baseline to follow‐up between the default mode network and the insula, cingulate cortex, temporal lobe, and somatosensory and motor cortices, were found in the CON group, but not in the WAD group. There were no changes post‐exercise in brain biochemistry. Conclusion: Aerobic and strengthening exercises did not exert differential effects on brain characteristics, however differences in structural and functional changes were found between WAD and CON groups. This suggests that an altered central pain modulatory response may be responsible for differential effects of exercise in individuals with chronic WAD. [ABSTRACT FROM AUTHOR]

Objective: To assess the potential of autophagy in migraine pathogenesis. Background: The interplay between neurons and microglial cells is important in migraine pathogenesis. Migraine‐related effects, such as cortical spreading depolarization and release of calcitonin gene–related peptide, may initiate adenosine triphosphate (ATP)‐mediating pro‐nociceptive signaling in the meninges causing headaches. Such signaling may be induced by the interaction of ATP with purinergic receptor P2X 7 (P2X7R) on microglial cells leading to a Ca2+‐mediated pH increase in lysosomes and release of autolysosome‐like vehicles from microglial cells indicating autophagy impairment. Methods: A search in PubMed was conducted with the use of the terms "migraine," "autophagy," "microglia," and "degradation" in different combinations. Results: Impaired autophagy in microglia may activate secretory autophagy and release of specific proteins, including brain‐derived neurotrophic factor (BDNF), which can be also released through the pores induced by P2X7R activation in microglial cells. BDNF may be likewise released from microglial cells upon ATP‐ and Ca2+‐mediated activation of another purinergic receptor, P2X4R. BDNF released from microglia might induce autophagy in neurons to clear cellular debris produced by oxidative stress, which is induced in the brain as the response to migraine‐related energy deficit. Therefore, migraine‐related signaling may impair degradative autophagy, stimulate secretory autophagy in microglia, and degradative autophagy in neurons. These effects are mediated by purinergic receptors P2X4R and P2X7R, BDNF, ATP, and Ca2+. Conclusion: Different effects of migraine‐related events on degradative autophagy in microglia and neurons may prevent prolonged changes in the brain related to headache attacks. [ABSTRACT FROM AUTHOR]

Background: The trigeminal vascular system is an important part of the anatomical and physiological basis of migraine. The effective connectivity (EC) among the regions of interest (ROIs) in the trigeminal vascular system involved in migraine without aura (MWoA) remains unclear. Methods: In this cross‐sectional study, 48 patients (mean [SD] age 38.06 [10.35] years; male, 14/48 [29%]) with MWoA during the interictal phase and 48 healthy controls of similar age and sex (mean [SD] age 38.96 [10.96] years; male, 14/48 [29%]) underwent resting‐state functional magnetic resonance imaging (fMRI). Dynamic causal modeling analysis was conducted to investigate directional EC among ROIs in the trigeminal vascular system including the bilateral brainstem, the primary somatosensory cortex (S1), the thalamus, and the insula. Results: Compared with the healthy control group, MWoA represented significantly reduced EC from the left brainstem (Brainstem.L) to the left insula (MWoA: mean [SD] −0.16 [0.36]; healthy controls: mean [SD] 0.11 [0.41]; Pcorrected = 0.021), reduced EC from the Brainstem.L to the right insula (MWoA: mean [SD] −0.15 [0.39]; healthy controls: mean [SD] 0.03 [0.35]; Pcorrected = 0.021), and decreased EC from the left thalamus (Thalamus.L) to the Brainstem.L (MWoA: mean [SD] −0.13 [0.56]; healthy controls: mean [SD] 0.10 [0.45]; Pcorrected = 0.021). Altered EC parameters were not significantly correlated with MWoA clinical data. Conclusion: These results further provide increasing evidence that disturbed homeostasis of the trigeminovascular nociceptive pathway is involved in the pathophysiological mechanisms of migraine. Patients with MWoA exhibited a regional interaction distinct from healthy controls in the neural pathway of the Bilateral Insula–Brainstem.L–Thalamus.L, which may shed light on the future understanding of brain mechanisms for MWoA. Future brain‐based interventions are suggested to consider the dysregulation in the Bilateral Insula–Brainstem.L–Thalamus.L circuits. [ABSTRACT FROM AUTHOR]