Background. Chronic low back pain (CLBP) is a clinically common and expensive disease. Patients frequently take sick leaves because of pain and dysfunction, and their unpleasant life and work experiences cause psychological depression and anxiety and affect their quality of life. Sleep disturbance is a common problem among patients with low back pain (LBP) with more than 50% complaining about poor sleep quality. This study aimed to explore the correlations between anxiety, sleep quality, and pressure-pain threshold (PPT) and their differences between patients with CLBP and asymptomatic people. Methods. Forty patients with CLBP and 40 asymptomatic people were recruited. Relevant data, including State-Trait Anxiety Inventory, Pittsburgh Sleep Quality Index, and PPT, were individually and independently collected by blinded physiotherapists with a practicing certificate and then statistically analyzed. An independent sample t-test was used to determine the intergroup differences between patients with CLBP and asymptomatic populations. Pearson correlation coefficient was employed for correlation analysis. Results. The CLBP group had significantly higher anxiety scores (41.64 ± 9.88 vs. 36.69 ± 8.31; t = −2.496, ) than the asymptomatic group. A significant difference was found in the total score of the Pittsburgh Sleep Quality Index (6.41 ± 2.43 vs. 5.09 ± 2.18; t = −2.628, ) but not in the trait anxiety (44.00 ± 7.83 vs. 42.67 ± 9.51; t = −0.695, ) of the two groups. State−Trait Anxiety Inventory showed a low to moderate negative correlation with PPT. No remarkable correlation was observed between Pittsburgh Sleep Quality Index and PPT. Conclusions. Patients with CLBP showed considerably worse state anxiety and sleep quality than asymptomatic people; however, no substantial difference in PPT was found between the two groups. The results suggest that in clinical practice, the focus should include pain and related social and psychological factors. CLBP treatment could be considered from multiple perspectives and disciplines.This trial is registered with Chinese Clinical Trial Registry (Trial registration: ChiCTR-TRC-13003701).

Purpose. The occurrence of low back pain (LBP) in marathon runners has been poorly understood. This study aimed to describe the risk factors and identify whether these factors can cause LBP in these athletes. Methods. A self-developed questionnaire was randomly distributed to 850 runners of running a half or a full marathon. Participants responded with the questionnaire focusing on previous training and running conditions after their competitions. Results. On the basis of the remaining 800 valid questionnaires, the incidence of LBP was 4.50% (n = 36). A total of 572 (71.5%) males and 228 (28.5%) females, with an average age range of 33.9 ± 9.0 years, came from different occupations with different physical activity characteristics. However, no significant associations between occupation and runners with LBP ( ) were found. In the final models, risk factors, including warm-up activities ( , OR = 2.617), fatigue (p = 0.008, OR = 2.680), running gait posture ( , OR = 2.273), and environmental temperature ( , OR = 6.584), were significantly associated with LBP in marathoners. Conclusion. Although LBP was uncommon in marathoners, it was linked to the factors such as insufficient warm-up activities, fatigue, poor running gait posture, and uncomfortable environmental temperature. Future studies need to validate these results. Nevertheless, these findings could still be useful for protecting the lower back area of runners clinically.

Objective: The aim of the study is to investigate the comparative effects of nonpharmacological therapies for managing global, attention, memory, and execution cognitive functions in stroke patients. Design: We searched PubMed, Embase, CINAHL, Cochrane Library, Web of Science, PEDro, and Google Scholar for randomized controlled trials that evaluated the effects of nonpharmacological therapies for treating stroke cognitive dysfunctions. We performed a network meta-analysis to estimate the mean treatment effect of 95% credible interval. Results: Seventy-three randomized controlled trials were included in the network meta-analysis for evidence syntheses. All therapies had significant effects than control on global cognition in stroke patients. Combined therapy was superior to other therapies for global cognition of all patients (vs. cognitive task therapy: 0.71, 95% credible interval = 0.14 to 1.29; vs. exercise: 0.88, 95% credible interval = 0.31 to 1.45, vs. physical modality therapy: 0.77, 95% credible interval = 0.16 to 1.40). Different therapies have effects on specific cognitive domains in stroke patients. Conclusions: Our findings suggest that nonpharmacological therapies are effective in improving global cognitive function in stroke patients, with cognitive task therapy, exercise therapy, physical modality therapy, and combined therapy being viable options (most optimal approach: combined therapy). Precise selection of therapies based on the time since stroke onset and specific cognitive domains can further enhance treatment outcomes.

Working memory deficits, one of the earliest hallmarks of Alzheimer’s disease (AD), are closely linked to abnormal neural activity in the dorsolateral prefrontal cortex (DLPFC). Transcranial direct current stimulation (tDCS), a non-invasive neuromodulation therapy, has been shown to ameliorate early AD working memory deficits by modulating excitatory activity in the DLPFC, yet the underlying mechanisms remain incompletely understood. This investigation was structured around 3 experimental phases. We initially applied tDCS to stimulate the left prefrontal cortex (PFC) of transgenic mice with 5 familial AD (5×FAD) 5 d per week for 4 weeks. Subsequently, we employed optogenetic (Opt) techniques to modulate left PFC glutamatergic neurons. Finally, we inhibited soluble N-ethylmaleimide-sensitive factor attachment receptor (SNARE) expression in the left PFC to elucidate the essential function of SNARE complex assembly with chaperone molecules in orchestrating synaptic vesicle release. tDCS treatment improved working memory deficits in early-stage AD mice. This was accompanied by increased cerebral blood flow, enhanced neuronal excitability, amelioration of neurochemical metabolic disorders, and reduced amyloid β-protein (Aβ) deposition in the left PFC. Opt stimulation of PFC glutamatergic neurons similarly improved working memory, indicating the association between tDCS’s therapeutic effects and synaptic plasticity of excitatory neurons. Crucially, tDCS facilitated synaptic vesicle fusion and release, evidenced by increased vesicle numbers, enhanced release probability, improved synaptic transmission efficacy, and upregulation of the SNARE complex, Snap25, and Syt1. Inhibiting SNARE expression in the left PFC attenuated the tDCS-induced improvements in synaptic vesicle release and working memory. These findings collectively demonstrate that left PFC-targeted tDCS modulates interactions between the SNARE complex and chaperone molecules, thereby promoting synaptic vesicle fusion and release. This mechanism underlies the amelioration of early AD-like working memory impairment by tDCS.