Neural Plasticity最新文献

[This corrects the article DOI: 10.1155/2013/954302.].

Neuroinflammation-induced cognitive impairment is characterized by a continued decline in memory, executive functioning, and information-processing abilities. Although berberine (BBR) exhibits anti-inflammatory and neuroprotective properties, its ability to mitigate cognitive deficits by regulating microglial-mediated neuroinflammation remains incompletely understood. To investigate the potential of BBR in mitigating microglial-mediated neuroinflammation and its detrimental effects on neuroplasticity and spatial memory, a mouse model was established through intrahippocampal microinjection of lipopolysaccharide (LPS). The results showed that BBR pretreatment significantly improved cognitive performance, suppressed microglial activation, reduced hippocampal neuronal damage, and increased the density of functional dendritic spines. Mechanistic analysis revealed that BBR treatment inhibited the phosphorylation of key proteins in the MAPK signaling pathway within microglia. These findings suggest that BBR is a promising therapeutic agent for mitigating neuroinflammation-induced cognitive impairment and provide significant evidence for its potential application in treating inflammation-related cognitive deficits.

[This corrects the article DOI: 10.1155/np/7939662.].

Objective: Attention is a critical cognitive function impaired in various neurological disorders, and brain-computer interface (BCI) training shows potential for cognitive improvement. However, the neural mechanisms of BCI training on attention networks remain unclear. This study investigated the effects of BCI training on attention and the underlying neural mechanisms in healthy young adults.

Methods: Thirty healthy young adults participated in this study. Attention function was assessed using the attention network test (ANT), while brain activation and connectivity were measured using functional near-infrared spectroscopy (fNIRS). Participants underwent the ANT and fNIRS assessments before and after BCI training.

Results: BCI training significantly improved the efficiency of the executive control network (p = 0.016). Nodal efficiency in the right posterior parietal cortex (PPC) was decreased (p  = 0.044). In the resting state, effective connectivity (EC) analysis showed decreased connectivity from the right PPC to the left PPC in the resting state (p  = 0.047). In the task state, the EC from the right prefrontal cortex (PFC) to the right PPC was significantly increased (p  = 0.016), and the connectivity from the left PFC to the right PFC was significantly decreased (p  = 0.023).

Conclusion: BCI training optimized connectivity within frontoparietal networks (FPNs), leading to enhanced executive control function. These findings suggest that BCI training could be an effective cognitive intervention for improving the function of FPNs. Future studies should explore the long-term effects of BCI training and its potential application in clinical populations, such as patients with attention deficit hyperactivity disorder and stroke.

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.

Astrocytes form an integral part of the nervous system and are proposed to modulate neuronal circuits and behavior. The motor cortex plays a key role in the planning and execution of voluntary movements and makes key contributions to motor skill learning. However, whether motor skill learning modulates astrocytic Ca²⁺ signaling in the primary motor cortex (M1) is not known. To understand the role of astrocytes in the M1, we first characterized the Ca²⁺ signaling properties in astrocyte subcompartments in awake mice. We found that the subcompartments exhibited different Ca²⁺ event properties during the no movement periods and locomotion. We then asked whether astrocytic Ca²⁺ signaling in M1 is modulated with the acquisition of a skilled forelimb reaching task. Astrocytes exhibited altered Ca²⁺ event properties at different stages of learning a forelimb reaching task, with early and transient increases in Ca²⁺ event amplitude being the most prominent. These results demonstrate for the first time that, in addition to previously described synaptic plasticity, astrocytic Ca²⁺ signaling is also modified with motor skill learning.

Global cerebral ischemia (GCI) during childhood is a leading cause of long-term cognitive impairment, yet no therapies currently exist to promote recovery in survivors. We previously demonstrated that juvenile mice exhibit transient hippocampal synaptic dysfunction after GCI, associated with reduced brain-derived neurotrophic factor (BDNF) expression and partial endogenous recovery over time. In this study, we tested whether delayed treatment with fluoxetine (FLX)-a selective serotonin reuptake inhibitor (SSRI) known to enhance BDNF-TrkB signaling-could accelerate synaptic recovery. Juvenile mice underwent cardiac arrest and cardiopulmonary resuscitation, followed by in vivo FLX or vehicle administration from postinjury days 10-13. Electrophysiological recordings on day 14 revealed that FLX restored hippocampal long-term potentiation (LTP) in males but not females. This effect was paralleled by an increase in hippocampal BDNF expression in FLX-treated males, whereas no change was observed in females. Paired ex vivo experiments further confirmed that acute FLX exposure rescued LTP in GCI-injured male slices. These findings suggest that FLX promotes synaptic recovery through BDNF-TrkB signaling in males, while recovery in females may proceed via alternate, hormone-dependent mechanisms. Together, these results identify a novel therapeutic window for enhancing neuroplasticity after juvenile GCI and underscore the importance of developmental stage and biological sex in shaping responses to treatment.

Background: Upper limb hemiplegia faces the challenge of slow and difficult recovery. A "closed-loop method" based on brain plasticity has been proposed, combining central and peripheral interventions to enhance the upper limb function. Based on the theory, we aimed to investigate the effect of transcranial direct current stimulation (tDCS) concurrent with virtual reality (VR)-based robotic intervention on upper limb recovery and cortical excitability.

Methods: In this single-blinded, randomized, controlled trial, 40 patients with subacute ischemic stroke were recruited and randomized to experimental (tDCS concurrent with VR-based robotic intervention) and control (sham tDCS concurrent with VR-based robotic intervention) groups. All patients received 15 sessions (20 min per day, 5 sessions per week). Outcome measures included the Fugl-Meyer Assessment Upper Limb Scale (FMA-UL), the Action Research Arm Test (ARAT), the Modified Barthel Index (MBI), and functional near-infrared spectroscopy (fNIRS).

Results: All 40 patients completed the intervention, with 34 included in the fNIRS analysis. FMA-UL (F = 22.239, p < 0.001) and ARAT (F = 10.984, p=0.002) scores showed significant time-by-group interaction effects. Greater improvements were observed in the experimental group compared to the control group for both FMA-UL (p < 0.001) and ARAT (p=0.001). MBI scores increased significantly in both groups over time (F = 55.415, p < 0.001), but the change scores did not differ significantly between groups (p=0.369). fNIRS analysis revealed a significant time-by-group interaction effect in the ipsilesional primary motor cortex (M1) (F = 4.762, p=0.037) and contralesional prefrontal cortex (PFC) (F = 10.881, p=0.002). Greater increases in activation were found in the experimental group for both ipsilesional M1 (p=0.025) and contralesional PFC (p=0.002).

Conclusions: Compared with sham tDCS concurrent with VR-based robotic intervention, tDCS concurrent with VR-based robotic intervention can effectively enhance upper limb function and promote activation of ipsilesional M1 and contralesional PFC in subacute ischemic patients with stroke. However, there was no obvious advantage in improving activities of daily life (ADL). Trial Registration: Chinese Clinical Trial Registry: ChiCTR2100047442.

Introduction: High-intensity readmill training (FAST) and functional electrical stimulation (FES) are both evidence-supported interventions that improve gait function post-stroke, but their neural mechanisms are unclear. Here, we tested the hypothesis that FAST-FES training, which incorporates task-specific sensorimotor stimulation to paretic ankle muscles, would induce greater upregulation of lesioned corticospinal tract (CST) excitability compared to dose-matched training without FES in individuals post-stroke.

Methods: In this repeated-measures crossover study, 11 participants >6 months post-stroke (66.25 ± 8.15 years, six females) received FAST-FES or FAST gait training protocols (comprising three training sessions) in a randomized order, with an intervening >3-week washout period. FES was applied to the paretic dorsi- and plantar-flexor muscles during the paretic swing and terminal stance phases of gait, respectively. CST excitability was measured before and after each training protocol from bilateral tibialis anterior and soleus muscles in three different test positions: sit-rest, sit-active, and quiet standing.

Results: We found a significant main effect of intervention on training-induced change in motor evoked potential (MEP) amplitude (p=0.02). Post hoc comparisons revealed that FAST-FES caused a larger training-induced increase in MEPs than FAST training (p=0.01). FAST-FES did not affect CST excitability of the nonlesioned hemisphere, with no significant changes in MEP amplitude of the nonparetic ankle muscles.

Conclusions: FAST-FES training increased corticospinal excitability in paretic ankle muscles without upregulating nonparetic ankle corticospinal drive, suggesting preferential induction of neuroplasticity in the lesioned CST.

Introduction: Music has long been recognized for its potential to modulate anxiety resistance at the population level. However, there is a lack of an auditory method that performs general and effective in enhancing anxiety resistance. Here we investigate the impact of a specific music that directly reflects brain activity (brain-wave music [BWM]) on anxiety resistance and its underlying neural mechanisms.

Method: A two-phase experimental protocol was designed utilizing the ToS anxiety induction paradigm to examine the efficacy of BWM in enhancing anxiety resistance. In Phase 1, resting-state EEG recordings were initially collected from 70 participants, followed by a standardized anxiety induction procedure involving auditory cues, to validate the effectiveness of the anxiety induction paradigm and establish baseline anxiety resistance for each participant. Phase 2, designed based on Phase 1 and conducted 24 h later, further investigated the neural mechanisms underlying anxiety regulation through brain-music intervention. Participants were randomly allocated into three groups: BWM (n = 30) group exposed to personalized EEG generated music, Preferred Music Control (PMC, n = 20) group to self-selected music, and silent control (SC, n = 20) to no auditory input. The anxiety induction procedure was then repeated in all groups. Anxiety levels were assessed through the state anxiety inventory (SAI) in both phases.

Results: Compared to Phase 1 resting-state baseline, the BWM group exhibited significantly reduced SAI scores in Phase 2, accompanied by enhanced prefrontal theta oscillations and functional connectivity between the prefrontal cortex, parietal lobe, and auditory cortex. No significant changes were observed in the other groups.

Discussion: These findings suggest that BWM effectively promotes anxiety resistance by facilitating network connectivity between the prefrontal and multisensory regions. Moreover, this study highlights BWM as a novel and promising method for emotional regulation.