NeuroImage最新文献

Objective: Dynamic PET imaging with ¹¹C-UCB-J enables in vivo quantification of synaptic vesicle glycoprotein 2A (SV2A), with prior reports of lower synaptic density in areas such as the brainstem nuclei and substantia nigra (SN) in Parkinson's disease (PD). Lowering PET dose reduces radiation exposure but increases noise and compromises quantification. This study evaluated a self-supervised two-step deep image prior (TS-DIP) denoising method for SV2A PET using 1/10 of the standard dose.

Methods: Thirty healthy controls (HCs) and 30 PD patients underwent 60-minute PET scans to acquire full-count list-mode data, later down-sampled into ten independent 1/10-count dynamic datasets. TS-DIP was applied to denoise reduced-dose frame images, and binding potential (BP_ND) maps were estimated. Performance was assessed by comparing group differences and correlations with motor severity against full-count results.

Results: Full-count data showed significant lower BP_ND in SN (-39%, p = 0.003) and red nucleus (RN; -27%, p = 0.009) in PD versus HCs. With 1/10-count data, SN differences remained significant, but RN differences were inconsistent. TS-DIP introduced minimal bias, restored statistical significance across all noise realizations, and improved recovery of correlations with motor scores (SN: r = -0.43 ± 0.02; RN: r = -0.42 ± 0.04) compared to raw 1/10-count data.

Conclusions: Dynamic SV2A PET imaging at substantially reduced doses is feasible when combined with advanced DL-based denoising techniques such as TS-DIP, supporting its potential for broader clinical application.

Many adolescents initiate social media use during early adolescence, but the associations of early social media use with neurodevelopment have not been extensively studied. We utilized neuroimaging data from the U.S. Adolescent Brain Cognitive Development (ABCD) Study to investigate the association of social media use (hours per day) or social media addiction (Social Media Addiction Questionnaire) with brain morphology in early adolescence. We analyzed data from 7,614 participants with high-quality structural MRI and complete covariate data at Year 2 (2018-2020, ages 10-13). In addition to pre-defined cortical regions, we performed vertexwise analysis using the Fast and Efficient Mixed Effects Algorithm (FEMA), which is unbiased by arbitrary borders between atlas-based brain regions and provides higher spatial resolution. After adjusting for demographics, socioeconomic factors, genetic ancestry, non-social media screen time, and scanner features, higher average daily social media use was significantly associated with lower total cortical thickness and volume. Region-of-interest (ROI) and vertexwise analysis identified broad regions with lower cortical thickness across the prefrontal cortices, temporal lobe, occipital lobe, and parietal lobe associated with social media use and social media addiction, which overlap with key nodes of the default mode network, prefrontal executive control networks, and visual processing and attention networks. Social media addiction was not significantly associated with differences in brain morphology in ROI analysis. Our findings in a large nationwide population demonstrate that higher social media use is associated with variation in cortical morphology, but future studies are required to establish the directionality of this association.

Potentially traumatic events (PTEs) and substance use (SU) are commonly endorsed in early adolescence, a crucial period for neurodevelopment. PTEs and SU are precipitating events in the etiology of comorbid posttraumatic stress disorder (PTSD) and substance use disorder (SUD). Separately, they have been shown to alter within- and between-network connectivity in the three brain networks posited by Menon's Theory of Psychopathology: the default mode network (DMN), fronto-parietal network (FPN), and salience network (SN). While comorbid PTSD+SUD in adulthood shows shared neural underpinnings, this is less clear in adolescence. We analyzed the effects of PTEs and SU on resting state functional connectivity (rsFC) in 9-15 year olds from the Adolescent Brain Cognitive Development (ABCD) Study. Fixed effects panel models were fit to assess the effects of PTEs and SU on between-network (FPN-SN rsFC, DMN-SN rsFC, and FPN-DMN rsFC) and within-network (FPN rsFC, SN rsFC, and DMN rsFC) connectivity measured across three timepoints spanning two years. PTEs, SU, and their interaction were not significantly associated with between- and within-network rsFC two years later. No sex specific interactions were observed. Results suggest rsFC changes observed in older adolescents and adults with comorbid PTSD+SUD do not developmentally translate to early adolescents endorsing PTEs+SU. Lack of impact on rsFC may indicate a potential buffer period in which PTEs and SU do not affect rsFC until later in development or after symptom onset following PTEs+SU.

Autobiographical memories enable us to "navigate" our personal past, although how the brain organizes them over extended time periods remains unclear. Using task-based fMRI and decoding analysis we found that a distributed network of areas in the brain, including medial temporal lobes, posterior parietal cortex, prefrontal regions, and visual association areas, distinguished memory age. The analysis of representational similarity matrices suggested that different regions contributed to the representation of the identity of unique events or their temporal representation. The right hippocampus encoded both fine-grained identity and temporal structure, whereas the frontopolar and retrosplenial cortices selectively encoded temporal structure. Representational connectivity analysis confirmed the robust inter-correlations within the right medial temporal lobe and prefrontal/retrosplenial cortex. These findings support the existence of a temporally organized mnemonic schema, namely a neural "timeline", that underlies our ability to situate and differentiate personal memories across the lifespan.

Problematic Usage of the Internet (PUI) is often characterized by deficits in inhibitory control. The links between such deficits and altered brain activity, though, have been fragmented and mixed. Thus, we seek here to identify communal patterns of brain activation related to inhibitory control in individuals with PUI through a comprehensive quantitative synthesis. To this end, we performed a systematic search of PubMed and Web of Science databases (March 2, 2025). It captured cross-sectional studies that (1) investigated whole-brain activation differences between PUI individuals and healthy controls during inhibitory control tasks, and (2) reported peak coordinates of significant differences. Out of 742 potentially relevant studies, 23 (comprising 548 PUI individuals and 537 healthy controls) were eligible for our analysis. They were subjected to anatomical likelihood estimation (ALE) meta-analysis using extracted coordinates. Results suggest spatial convergence in the left middle frontal gyrus and the right superior parietal lobule. These brain regions mediate executive control and top-down regulation. We conclude that the observed increased activation in the left middle frontal gyrus and right superior parietal lobule during inhibitory control tasks is a neural pattern that is often associated with PUI. Neurotransmitter enrichment analysis revealed that this brain activation pattern in PUI individuals was negatively associated with 5-HTT distribution, implicating a potential involvement of serotonergic systems in inhibitory control alterations. Further investigations are needed to elucidate the nature of brain activation differences across various PUI subtypes, establishing causality, and generalizability to other samples.

Background: Children of parents with mental illness (at-risk) face an increased risk for developing mental health issues themselves than children of healthy parents (controls), yet the neurobiological underpinnings remain unclear. This study explored differences in white matter (WM) between at-risk children and controls, focusing on brain pathways related to emotion regulation and the associations between parenting behaviours, stress, and WM microstructural properties.

Methods: WM properties were assessed via diffusion-weighted imaging in 64 children (28 at-risk, 36 control) across five emotion-related pathways. Multiple regression analyses examined pathway alterations between groups and associations between parenting behaviours, parenting stress, emotion regulation and WM pathways across all participants beyond effects of group membership, controlling for socioeconomic status, age, sex, scanning site and global WM volume.

Results: At-risk children showed alterations in the right inferior longitudinal fasciculus (ILF), indicated by higher fractional anisotropy and lower mean diffusivity. Across groups, dysfunctional parenting was associated with widespread WM alterations, including the corpus callosum (CC) genu, bilateral dorsal cingulum, bilateral ILF, in parts of the superior longitudinal fasciculus and left uncinate fasciculus. Additionally, lower partnership support was specifically linked to alterations in the CC genu. No significant associations were found between WM microstructure and children's self-reported emotion regulation.

Conclusions: These findings show potential evidence of altered WM pathways in children at-risk for mental illness, particularly in emotion regulation related pathways. Additionally, parenting behaviour and stress were associated with WM microstructure in children, underscoring potential influence of early environmental factors on brain development. Longitudinal and replication studies are needed to clarify causal mechanisms and long-term effects.