IntroductionSleep supports memory consolidation through the reactivation of neural circuits engaged during learning. Targeted Memory Reactivation (TMR), in which memory-associated sensory cues are presented during sleep, can enhance declarative memory retention. However, the neural signatures supporting odor-cued reactivation remain incompletely characterized.Materials and methodsHere, we analyzed high-density electroencephalography (EEG) recordings from a TMR paradigm designed to dissociate neural responses associated with declarative and non-declarative odor cueing during sleep. EEG epochs were examined across fast- (12.5–16 Hz) and slow-spindle (9–12.5 Hz) frequency bands, channel subsets (all, frontal, central, and posterior), and multiple post-cue time windows (0–2, 0–4, and 0–7 s). Using within-participant machine learning based on Riemannian geometry, we classified EEG epochs elicited by a declarative memory-associated odor (Odor D) vs. vehicle control, and by a non-declarative odor associated with a motor task (Odor M) vs. vehicle.ResultsDecoding performance relative to permutation-derived chance showed condition-dependent patterns across frequency bands, time windows, and channel subsets. Across analyses, decoding tended to be higher in the declarative condition (Odor D) than in the non-declarative condition (Odor M), with the strongest effects observed in central channels. Channel-level contribution analysis further indicated more spatially structured covariance patterns during Odor D over central regions, whereas contributions during Odor M were more diffuse and less consistent. These effects were modest and did not survive correction for multiple comparisons.DiscussionThese results suggest that declarative odor cueing during sleep is associated with more structured spindle-band EEG patterns than non-declarative cueing, particularly over central channels, although effects were modest and did not survive correction for multiple comparisons. A key finding is a difference in central-channel contribution patterns between conditions, consistent with memory-related neural modulation. These findings also highlight the potential of covariance-based decoding approaches for probing distributed sleep EEG dynamics, warranting further validation in larger samples.
Editorial: Advancing neurodegenerative disease biomarkers: the role of neuroimaging in TDP-43 and tau proteinopathies
Relationship between spontaneous EEG oscillations at 7 and 45 days of acute plateau exposure and the plateau acclimatization index
IntroductionThis study tracked 47 high-altitude migrants to investigate the adaptive mechanisms of the brain to hypoxic environments.MethodsEEG and physiological indicators (SpO2, HCT, AAI) were recorded during the acute (7 days) and chronic (45 days) phases of high-altitude exposure. EEG complexity was assessed using multiscale entropy (MSE), and inter-regional brain coupling was also analyzed.ResultsCompared with the chronic phase, EEG complexity in the frontal, parietal, and occipital lobes was higher in the acute phase, whereas inter-regional brain coupling was stronger in the chronic phase. SpO2 decreased during the acute phase and then slowly recovered; HCT continued to rise; AAI showed a decelerating downward trend. Correlation analysis revealed that SpO2 was negatively correlated with fine-scale MSE, and HCT was negatively correlated with medium- to coarse-scale MSE. AAI was correlated only with occipital MSE during the acute phase. During the chronic phase, AAI was negatively correlated with MSE coupling across multiple brain regions but not with MSE itself.DiscussionThese findings suggest that hypoxia may increase fine-scale complexity by enhancing local neural interconnections, whereas elevated HCT reduces long-range interactions between distributed neural populations. The brain exhibits a compensatory pattern of “complexity reduction with enhanced inter-regional coupling” during hypoxic adaptation, which may represent an optimization of neural efficiency under sustained hypoxia.
Transcranial magnetic stimulation and motor overflow: a systematic review in neurological disorders
Motor overflow, a neuromotor phenomenon characterized by involuntary activation of muscles during voluntary movement, reflects impairments in interhemispheric and intracortical inhibition and is commonly observed in conditions such as stroke, cerebral palsy, dystonia, and Parkinson’s disease. Transcranial Magnetic Stimulation (TMS) is a non-invasive neuromodulatory technique with potential to modulate the cortical excitability underlying overflow-related dysfunctions. This systematic review aimed to evaluate the efficacy of TMS in reducing motor overflow across neurological populations. Seven randomized controlled trials (RCTs) were included, encompassing participants with stroke, cerebral palsy, Parkinson’s disease, and focal hand dystonia. Protocols varied in frequency (1–10 Hz), target area (M1, SMA, PSC, PMC), and design (e.g., crossover, combined protocols with constraint-induced therapy or cerebellar stimulation; Motor overflow was directly assessed in only two studies, one involving Parkinson’s disease and one involving dystonia, thereby limiting cross-study comparisons. Therefore, evidence supporting a direct effect of TMS on motor overflow remains preliminary and condition-specific. In dystonia, high-frequency rTMS (10 Hz) targeting the primary somatosensory cortex led to significant reductions in overflow, demonstrated by handwriting kinematics. In Parkinson’s disease, although physiological modulation (reduced IHI) was observed after SMA stimulation, mirror movements remained unchanged. In stroke and cerebral palsy populations, overflow was not directly evaluated, though improvements in motor function, spasticity, and cortical excitability were consistently reported. Risk of bias was low in most included studies, although gaps in allocation reporting and standardization of outcome measures were noted. This review highlights the potential of TMS, particularly high-frequency protocols, to modulate motor overflow in focal dystonia. However, the lack of targeted assessment in other neurological conditions suggests a critical need for future trials with standardized protocols and specific outcome measures focused on overflow to clarify the therapeutic role of TMS in rehabilitation.
Neuroprotective effects of paederoside against mitochondrial dysfunction in rotenone-induced cell models of Parkinson’s disease
IntroductionParkinson’s disease (PD) is the second most prevalent neurodegenerative disorder and is one of the leading causes of neurological disability. Although there are currently no cures or treatments for this disease, many patients with PD may therapeutically benefit from preventing or mitigating mitochondrial dysfunction. This study aimed to investigate the protective effects of paederoside against rotenone-induced neuronal damage in Neuro-2A (N2A) cell models of PD.MethodsFirst, the cytotoxic effects of rotenone on N2A cells were assessed using the cell counting kit-8 assay to establish a cell model of PD. Second, the effects of paederoside on mitochondrial complex I activity, mitochondrial swelling, and caspase-3 activity in the rotenone-induced cellular model were investigated. Finally, the impact of paederoside on tyrosine hydroxylase-positive cells in a rotenone-induced co-culture of N2A cells and BV-2 cells (N2A/BV-2) was studied.ResultsN2A cells were significantly damaged by rotenone in a time- and concentration-dependent manner; a 48 h rotenone treatment at 20 nM was used to create a cell model of PD. Pretreatment with 1 μM paederoside notably increased mitochondrial complex I activity in N2A cells with rotenone-induced impairment, leading to 42.85% increase. Additionally, pretreatment with 0.1, 1, and 10 μM paederoside considerably alleviated rotenone-induced mitochondrial swelling as indicated by the optical density (OD) (10 min)/OD(0 min) ratio, which increased by 1.21-, 1.33-, and 1.37-fold, respectively. Notably, pretreatment with 10 μM paederoside significantly inhibited caspase-3 activation triggered by rotenone in this cellular setting, resulting in a 39.93% decrease in enzyme activity. Moreover, pretreatment with 10 μM of paederoside markedly enhanced the number of TH-positive cells in a co-culture system consisting of N2A/BV-2 cells induced by rotenone, with increases of 82.79%.ConclusionPretreatment with paederoside may protect against mitochondrial dysfunction in cell models of PD induced by rotenone.
Case Report: Subacute combined degeneration misdiagnosed as a primary affective disorder: diagnostic pitfalls and clinical red flags
BackgroundSubacute combined degeneration (SCD) of the spinal cord is a progressive neurological disorder caused by vitamin B12 deficiency. When initial symptoms present as nonspecific fatigue, dizziness, and affective distress, the condition is frequently misattributed to primary psychiatric disorders. This “diagnostic overshadowing” leads to critical delays in administering definitive therapy, risking irreversible axonal damage.Case presentationA 39-year-old male presented with a nine-month history of progressive paresthesia, dizziness, and emotional distress. Initial medical workups (including brain CT and EEG) were unremarkable, leading to a diagnosis of Somatic Symptom Disorder and anxiety. Despite treatment with multiple psychotropic agents, his condition deteriorated, eventually manifesting as lower limb weakness and significant gait ataxia. Subsequent evaluation at a tertiary center revealed absent patellar reflexes and impaired vibratory sensation. Psychometric testing (SCL-90) showed a high somatization factor (3.00). Investigations confirmed a critically low serum vitamin B12 level (<37 pmol/L) and characteristic longitudinally extensive T2-weighted hyperintensities in the dorsal columns from C3 to T12. Following intramuscular and oral vitamin B12 replacement, supplemented by escitalopram for residual distress, the patient achieved significant recovery. At five-month follow-up, he was fully ambulatory with near-normalization of psychometric scores.ConclusionThis case illustrates the risk of misinterpreting organic neurological deficits as psychogenic somatization. A discrepancy between subjective psychiatric complaints and emerging objective neurological signs-such as absent reflexes or ataxia-should trigger an immediate search for underlying organic etiologies and the initiation of targeted treatment.
Virtual reality based attentional bias modification training for patients with obsessive-compulsive disorder: a feasibility study
BackgroundAttentional bias modification (ABM) training is employed to modulate attentional bias and alleviate clinical symptoms in obsessive-compulsive disorder (OCD) patients. This study aimed to develop a novel, ecologically valid ABM paradigm based on virtual reality (VR). The intent was to enhance the efficacy of traditional computerized ABM and to preliminarily examine its feasibility in patients with contamination-based obsessive-compulsive disorder (OCD).Method15 patients with OCD who were currently receiving pharmacotherapy were recruited and allocated to either an ABM group, which received VR-ABM training twice weekly for four weeks (eight sessions in total), or a TAU group, which continued their routine outpatient treatment, including pharmacotherapy, psychotherapy, and physical therapy.Result5 patients in ABM group and 5 patients in TAU group completed the 4-week follow-up. VR-ABM paradigm effectively elicited target symptoms, with virtual scenarios inducing moderate levels of obsessive-compulsive symptoms and anxiety. Notably, all participants in the VR-ABM group reported the program to be appropriately challenging, effectively eliciting obsessive-compulsive symptoms and improving subjective concentration.ConclusionThese preliminary findings support the feasibility of the novel VR-ABM training in OCD and warrant further investigation in larger, controlled trials to rigorously evaluate its therapeutic efficacy.
Systematic review of animal studies on the use of herbal medicine for attention-deficit/hyperactivity disorder
BackgroundAttention-deficit/hyperactivity disorder (ADHD), a common neurodevelopmental condition, often requires treatment with stimulants such as methylphenidate and nonstimulants such as atomoxetine. Despite their effectiveness, medication-related side effects, adherence and symptom control issues have increased the interest in alternative therapies, especially herbal medicine. However, existing preclinical studies vary in quality and relevance. This systematic review evaluates animal studies investigating herbal medicines for ADHD; identifies limitations in experimental models, behavioral assessments, safety evaluation, and methodological rigor; and proposes a framework to guide future research.MethodsFollowing PRISMA 2020 guidelines, PubMed and Web of Science were systematically searched for eligible studies published between 1995 and March 2025 that used animal models to interventions for the treatment of ADHD-like symptoms.ResultsAnalysis of 25 studies revealed a strong reliance on a limited range of animal models, particularly the spontaneously hypertensive rat (48%), with 88% of studies using male animals exclusively. Behavioral assessments predominantly focused on hyperactivity (72%), whereas evaluations of inattention and impulsivity were comparatively limited. Herbal interventions were associated with improvements in ADHD-like behaviors and modulation of catecholaminergic neurotransmission, including increased dopamine and norepinephrine levels in the prefrontal cortex. Additional mechanisms included activation of neurotrophic signaling pathways (brain-derived neurotrophic factor/TrkB) and suppression of proinflammatory mediators such as TNF-α and IL-1β. However, 80% of the studies did not report safety outcomes, and no study clearly described randomization or blinding procedures, limiting the translational relevance of the findings. Despite these limitations, several formulations, including the Long Mu Qing Xin mixture, An Shen Ding Zhi Ling demonstrated promising multitarget effects.ConclusionAlthough herbal medicines demonstrate promising multipathway effects for ADHD, progress remains constrained by the limited diversity of animal models and narrow scope of behavioral assessments. Future research should prioritize the use of diverse models, more comprehensive assessments, and the implementation of rigorous methodological standards.
Job demands and resources in relation to burnout and educational coexistence among Chilean education workers
This study aimed to examine the fit of a structural equation model relating selected job demands and job resources to burnout and perceptions of educational coexistence among Chilean education personnel. A total of 710 workers from this sector (administrators, teachers, and teaching assistants) participated. Structural equation modeling (SEM) was conducted using robust maximum likelihood estimation and absolute and incremental fit indices. The proposed model showed acceptable fit (χ² = 3181, df = 1307, p <.001; CFI Robust = 0.911; TLI Robust = 0.907; GFI = 0.956; RMSEA Robust = 0.049). Workload and work-family conflict were positively associated with burnout (R² = 0.612; p <.001), whereas role clarity and social support were positively associated with perceptions of educational coexistence (R² = 0.396; p <.001). Overall, the findings are consistent with the Job Demands-Resources framework and suggest that, in this sample, job demands are more strongly linked to burnout, whereas job resources are more strongly linked to perceptions of educational coexistence. The study is discussed in relation to the Chilean educational context and the implementation of the National Policy on Educational Coexistence.
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