Neural Plasticity最新文献

Aim: Diffusion tensor imaging-analysis along the perivascular space (DTI-ALPS) indicators and free-water (FW) mapping derived from diffusion tensor imaging (DTI) data have been proposed as noninvasive markers of glymphatic system (GS) function. This study aimed to investigate GS function in children with sensorineural hearing loss (SNHL) with particular focus on the sensitive period of auditory development.

Methods: This study enrolled 53 children with SNHL (SNHL group) and 42 age- and sex-matched healthy children (healthy control [HC] group). Based on the age of 36 months, we separated the study participants into two groups: Group A (0-36 months; A-SNHL group, n = 32; A-HC group, n = 21) and group B (36-180 months; B-SNHL group, n = 21; B-HC group, n = 21). We collected their DTI image data and calculated the ALPS index for the left and right hemispheres and the fractional volume of free water in white matter (FW-WM) and analyzed the differences between the groups. The DTI-ALPS has several limitations, the most prominent one being the influence of microstructure. However, it has many advantages and high clinical value.

Results: Compared to the HC group, the ALPS index for both hemispheres in the SNHL group was significantly lower (L: p < 0.001; R: p < 0.001), and group B exhibited the same results (L: p < 0.001; R: p < 0.001). In group A, the left-hemisphere ALPS index of the A-SNHL group was significantly lower than that of the A-HC group (L: p = 0.002; R: p = 0.067). The FW imaging analysis indicated that the FW-WM in the B-SNHL group was significantly higher than that of the B-HC group, and it exhibited a negative correlation with the left-hemisphere ALPS index (r = -0.515, p = 0.017).

Conclusion: Children with SNHL (especially those over 3 years old) might exhibit compromised cerebral glymphatic function, possibly attributable to clearance dysfunction and interstitial fluid (ISF) retention. Despite the recognized limitation of DTI-ALPS, its integration with FW mapping may enhance the noninvasive indirect evaluation of glymphatic function.

Various forms of mild stress may exacerbate pain in patients with chronic pain disorders, though the underlying mechanism remains unclear. Astrocyte activation in the spinal dorsal horn plays a predominant role in stress and pain. The present study investigated the neuron-astrocyte interactions in the spinal dorsal horn in post-traumatic stress disorder (PTSD)-induced hyperalgesia using a single-prolonged stress (SPS) model, a Complete Freund's Adjuvant (CFA) model and an SPS + CFA model. Animals were tested for mechanical withdrawal threshold (MWT) of the paw after SPS, CFA and SPS + CFA. SPS + CFA group induced significantly increased mechanical allodynia compared with the SPS or CFA group. We tested the hypothesis that IL-1β contributes to signaling between astrocytes and neurons in stress-induced hyperalgesia (SIH). Immunohistochemical data showed that there was an upregulation of glial fibrillary acidic proteins (GFAPs, a marker of astrocyte) and Fos (a marker of neuron) in SIH. Immunohistochemical data showed specific localization of IL-1β to astrocyte, but not to microglia and neurons and a neuronal localization of the IL-1β receptor (IL-1RI) with NMDAR2B (NR2B). Enzyme immunoassay analysis showed that IL-1β release was dependent on c-Jun N-terminal kinase (JNK) activation in astrocyte. The JNK inhibitor SP600125 suppressed IL-1β release. SP600125 and IL-1RI blockade with IL-1ra resulted in a restoration of behavioral nociceptive thresholds. Our results showed that the IL-1β-dependent, JNK-regulated astrocyte-neuron signaling pathway mediated the astroglia component of pain maintenance in SIH.

Objective: The central auditory system has greater plasticity when children are 2-4 years old, called the auditory sensitive period, during which cochlear implantation (CI) can give a good prognosis to children with congenital sensorineural hearing loss (CSNHL), but some will have a poor prognosis. This experiment aims to construct a structural brain network by using diffusion tensor imaging (DTI) and analyze alterations of the topological properties of structural brain networks by graph theory method, provide an imaging basis for the pathophysiological mechanism of white matter network changes with age in SNHL children.

Materials and methods: A total of 109 children with SNHL and 61 normal control groups were included. According to the auditory sensitivity period, children were divided into a group within the auditory sensitivity period (group A, 12-47 months) and a group beyond the auditory sensitivity period (group B, 48-120 months). DTI data were collected to construct the structural brain network for graph theory analysis, identify the network changes of the topological properties of the SNHL, as well as the differences before and after the auditory sensitivity period.

Results: Compared with the control group, both groups of SNHL had network topological changes. Group A showed a decrease in nodal parameters in higher-order cognitive-related brain regions but no difference in global topology parameters and network connection strength. However, group B showed a decrease in the nodal parameters of multiple contact cortical brain regions and the global efficiency (Eglob) of structural networks. Besides, subnetwork analysis showed weakened connection strength between key brain regions related to higher-order cognition.

Conclusion: The structural brain network of SNHL children before the auditory sensitive period has not undergone extensive changes, and once the auditory sensitive period of development is exceeded, the formation of deaf brain features will be more obvious, with greater impact on higher-order cognitive regions. Before the auditory sensitivity period, hearing stimulation should be introduced to SNHL children as soon as possible to reduce extensive damage to the white matter network.

This study examined the correlation between the cerebellar functional status and the executive function (EF) scores and explored alterations of functional connectivity (FC) among autism spectrum disorder (ASD) individuals compared to typically developing (TD) subjects. Individuals from the Autism Brain Imaging Data Exchange II dataset (ABIDE II) with complete cerebellum scanning coverage and available Behavior Rating Inventory of EF (BRIEF) t-scores were included, yielding a final sample of 71 ASD (age: 11.50 ± 2.77) and 149 TD (age:11.48 ± 1.60) individuals. Four cerebellar ROIs (left Lobule VI, left Crus I, right Crus I, and left VIIB) were defined from a meta-analysis. We quantified cerebellar intrinsic activity using percent amplitude of fluctuation (PerAF) and assessed seed-based FC within cerebro-cerebellar circuits. We found no between-group differences in PerAF across the four ROIs, and PerAF showed no significant association with global executive composite (GEC) scores within the ASD group. In contrast, FC analyses revealed predominantly increased cerebro-cerebellar connectivity in ASD. Notably, stronger FC between left Lobule VI and right inferior frontal gyrus, pars opercularis (IFGoper), as well as between left Crus I and left IFGoper were positively correlated with BRIEF Shift scores, indicating that greater coupling within these loops was associated with poorer cognitive flexibility. These results suggest that EF impairment among ASD individuals might be reflected in part by alterations in functional interconnections within the cerebro-cerebellar system. These findings help to understand the potential role of the cerebellum in EF among ASD individuals and might provide ideas for therapeutic interventions.

Alzheimer's disease (AD) is a progressive and debilitating neurodegenerative disorder for which existing pharmacotherapies are inadequate to arrest pathological progression, highlighting the imperative to identify safe and effective nonpharmacological interventions. Exercise, as a multi-target therapeutic modality, has been shown to reverse multiple facets of AD-related neuropathology through diverse mechanisms. In this systematic review, we synthesize evidence on the effects of voluntary running, structured swimming, and modulation of the gut microbiota in transgenic murine models of AD. Exercise was found to ameliorate AD pathology by modulating amyloid precursor protein (APP) processing and β-amyloid (Aβ) production/clearance, restoring mitochondrial integrity and function, attenuating neuroinflammatory responses, enhancing synaptic plasticity, and upregulating neurotrophic factors. Moreover, exercise reshapes the intestinal microbiome and thereby modulates the gut-brain axis, further promoting neuroimmune homeostasis and cognitive resilience. Through RNA sequencing data analysis, key genes such as Tlr4, Cdc42, and F13a1 were identified, which may play significant roles in neuroimmune regulation and cognitive protection. By integrating multi-omics evidence, we propose a coordinated "exercise-microbiota-brain" mechanistic framework that offers theoretical support for personalized, exercise-based therapeutic strategies and translational applications in AD. We also emphasize the necessity of future studies combining exercise with complementary interventions to accelerate the clinical translation of multimodal therapeutic approaches.

Exercise training plays a pivotal role in neural repair and secondary injury prevention following spinal cord injury (SCI) and is widely implemented in clinical rehabilitation. It induces adaptive changes and remodeling within the nervous system of SCI patients, thereby improving functional impairments. The mechanisms underlying this adaptive remodeling involve complex signaling pathways, with mechanosensation and mechanotransduction being indispensable. Mechanosensitive ion channels (such as Piezo channels) sense and transduce mechanical forces generated during exercise, triggering downstream biochemical reactions that regulate cellular functions and ultimately promote functional recovery. This review systematically synthesizes evidence from Piezo channel-related animal studies and clinical research, focusing on their role in reshaping the structure and function of the nervous system through exercise intervention post-SCI. The study aims to elucidate the molecular mechanisms by which Piezo channels mediate exercise-induced functional recovery after SCI, providing a theoretical foundation for developing precision exercise prescriptions to facilitate functional reconstruction and rehabilitation in patients.

Background: Resting-state functional magnetic resonance imaging (rs-fMRI) reveals diverse neural activity patterns in adolescent major depressive disorder (MDD) with nonsuicidal self-injury (NSSI; nsMDD). However, the reported results are inconsistent. The aim of this study was to conduct a meta-analysis to identify consistent patterns of brain activity alterations in adolescent nsMDD.

Methods: A systematic search was conducted across PubMed, Web of Science, Embase, Google Scholar, Wanfang, and CNKI for rs-fMRI studies that compared nsMDD patients with healthy controls (HCs), up to June 30, 2025. Significant cluster coordinates were extracted for comprehensive analysis. We utilized regional homogeneity (ReHo) and amplitude of low-frequency fluctuations (ALFFs) analyses. Activation likelihood estimation (ALE) was used to identify regions of aberrant spontaneous neural activity in adolescent nsMDD compared to HCs.

Results: Eight studies (249 adolescent nsMDD and 278 HCs) were included. The ALE meta-analysis revealed increased activity in the left lingual gyrus (LING; Brodmann area [BA] 18) in adolescent nsMDD compared to HCs (voxel size = 200 mm³; p < 0.05). Decreased activity was observed in the right posterior cingulate cortex (PCC; BA 29) in adolescent nsMDD compared to HCs (voxel size = 360 mm³; p < 0.05). Jackknife sensitivity analyses demonstrated robust reproducibility in five of eight tests for the left LING and in six of eight tests for the right PCC.

Conclusions: This meta-analysis confirms consistent alterations in specific brain regions in adolescent nsMDD, highlighting the potential of rs-fMRI to refine diagnostic and therapeutic strategies.

Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by Aβ-amyloid accumulation and cognitive decline. Despite extensive research, effective treatments remain elusive. Astrocytes, the most abundant glial cells, play a crucial role in synaptic transmission, neuronal excitability, and plasticity. In AD, astrocytes become reactive, exhibiting aberrant calcium signaling and altered neurotransmitter release, making them promising targets for disease-modifying therapies. To address this, we explored designer receptors exclusively activated by designer drugs (DREADDs), specifically the hM3D(Gq) receptor, which selectively modulates intracellular Ca²⁺ levels in astrocytes upon activation by clozapine-N-oxide (CNO). Using daily CNO administration in 8-month-old 5xFAD mice, we observed a significant enhancement of impaired long-term potentiation formation, accompanied by cognitive improvements in the fear conditioning (FC) and Morris water maze (MWM) tests. Additionally, anxiety levels and social preference deficits in 5xFAD mice were fully restored following astrocytic activity modulation. Importantly, this approach reduced Aβ-amyloid plaque burden and demonstrated a trend toward mitigating astrocytic reactivity, further highlighting its therapeutic potential. Our findings suggest that targeting astrocytic activity via Gq-coupled receptors represents a novel and promising strategy for AD treatment, offering a noninvasive and effective approach to mitigating disease progression.

Peripheral nerve injury (PNI) represents a prevalent clinical condition, often resulting from mechanical trauma or tumor resection, which frequently induces persistent sensory deficits, motor impairment, neuropathic pain, or paralysis. Consequently, substantial socioeconomic burdens are imposed on affected individuals. Autologous nerve transplantation is often considered the preferred approach for reconstructing peripheral nerve defects; however, this technique is associated with limitations including donor-site sensory loss, restricted graft length, and nerve mismatches. Recently, peripheral blood mononuclear cells (PBMCs) have emerged as a focal point in nerve regeneration research due to their accessibility, immunomodulatory properties, and neuro-reparative potential. Nevertheless, the precise mechanisms underlying PBMC-mediated nerve repair remain incompletely characterized, and their molecular pathways require further elucidation. This study explores the potential role of PBMCs in promoting peripheral nerve regeneration, with a particular focus on their regulation of retrograde brain-derived neurotrophic factor (BDNF) transport through modulation of Hook1 expression and associated molecular pathways. This research seeks to provide novel insights for PBMC-based therapeutic strategies and establish a theoretical foundation for clinical translation. Implementation challenges and translational prospects for PBMCs in nerve regeneration are also critically evaluated.