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17 papers

Hearing Loss in Adults With Diabetes and Prediabetes: A Systematic Review and Meta-Analysis.

Nisar M et al. · Jul 1, 2026

Diabetes impairs hearing through microvascular damage and neuropathy, yet the prevalence of moderate-to-severe hearing loss (≥ 40 dB HL) remains inadequately explored. Variations by age, diabetes duration, and socioeconomic factors are inadequately characterised. This systematic review quantified the prevalence and comparative risk of moderate-to-severe hearing loss in diabetes and prediabetes, exploring variations across age, national income level, and disease duration. We searched PubMed, Scopus, Web of Science, SPORTDiscus, and CINAHL (2000-2025) for observational studies reporting audiometric thresholds in diabetic or prediabetic subjects (PROSPERO: CRD42018100742). Quality was assessed using the Newcastle-Ottawa Scale. Random-effects meta-analyses generated pooled prevalence and odds ratios (ORs) with 95% confidence intervals (CIs). Publication bias was evaluated via funnel plots and Egger's regression. Of 3490 records, 29 studies qualified. Most examined type 2 diabetes; one included prediabetes. Twenty-three studies (n = 5221) yielded a pooled prevalence of 24% (95% CI: 19%-30%; I 2 = 94%). Eleven studies showed diabetes doubled hearing loss odds versus controls (OR = 2.41, 95% CI: 1.62-3.60; I 2 = 86.6%). Risk was significantly elevated in younger adults (< 60 years: OR = 3.03, 95% CI: 2.17-4.22) but not in older adults (≥ 60 years: OR = 1.52, 95% CI: 0.72-3.22). Low- and middle-income countries showed the highest risk (OR = 4.51, 95% CI: 2.43-8.40) versus high-income countries (OR = 1.78, 95% CI: 1.05-3.02). Diabetes duration < 10 years conferred elevated risk (OR = 2.68). Small-study effects were detected (Egger's p = 0.019) but sensitivity analyses confirmed robustness. One in four diabetic adults has clinically significant hearing loss, particularly in younger individuals and resource-limited populations. These findings support the integration of routine audiometric screening into diabetes care.

Neuroscience

The Orexin System Modulates Stress-Induced Alcohol Preference and Reinstatement in Adolescents: Bioinformatics and Experimental Evidence.

He W et al. · Jul 1, 2026

Underage drinking has become a global public health concern. One of the major causes of underage drinking is stress. The orexin system has been reported to be involved in both alcohol addiction and stress. However, few studies have examined this system, especially among adolescents. Therefore, we constructed protein-protein interaction (PPI) networks to confirm that orexin receptors are connected to stress- and alcohol dependence-related genes, providing a theoretical basis for our experimental approach. Animal experiments employed the conditioned place preference (CPP), the foot-shock stress model and the enzyme-linked immunosorbent assay (ELISA), to elucidate the role of the orexin system in the stress-induced alcohol addiction-related behaviour among adolescent mice. Our results revealed that there were interactions among orexin system, chronic/acute stress and alcohol dependence related proteins. Otherwise, chronic stress can increase the animals' vulnerability to alcohol addition-related behaviour. Additionally, acute foot-shock can promote alcohol-seeking behaviour reinstatement and facilitate orexin concentrations in brain regions that have been shown to be associated with reward and addiction. Moreover, the inhibition of orexin receptors can attenuate the formation and reinstatement of alcohol addiction-like behaviour among adolescent mice. Collectively, our findings indicate that orexin system may be a pivotal target for preventing stress-induced alcohol addiction and reinstatement among the adolescents.

Neuroscience

A Single Session of Slackline Training Induces Rapid, Task-Specific Balance Improvements and Elevated Resting-State Beta Band Power.

Kenville R et al. · Jul 1, 2026

Balance training underpins both sports performance and rehabilitation, while its efficacy depends on the amount of training and task difficulty. Here, we characterized neurophysiological changes accompanying the earliest phase of slackline-specific balance acquisition within a closely matched active-control design. For this purpose, 35 healthy, slackline-naïve adults were randomized to a slackline intervention or a time-matched active control. Before and after training, participants completed slackline single-leg stance with eyes open (SL-EO) and eyes closed (SL-EC), resting-state electroencephalography (EEG), and tibial-nerve somatosensory-evoked potentials (SEP). EEG band-specific power was quantified after aperiodic correction and resulting change scores were analyzed with non-parametric mixed models. The intervention group showed larger gains in SL-EO than control, whereas SL-EC showed no between-group difference. Resting-state EEG exhibited a band-specific pattern with a greater post-training increase in beta power in the intervention group, whereas alpha and theta showed no selective group effects. SEP amplitudes did not change pre-post in either group. Finally, within the intervention group, beta power change did not correlate with individual performance gains. Overall, the present study revealed that resting-state beta power was sensitive to the earliest phase of slackline-specific balance acquisition, whereas tibial-nerve SEP amplitudes remained unchanged. These findings suggest that resting beta power may capture acute post-practice sensorimotor network changes after a single session of slackline training. Future work should assess generalizability across tasks and populations, combine task-based EEG with resting measures to link brain state to on-task control, and track if SEP changes arise over practice to refine models of balance learning.

Neuroscience

Early Life Stress Affects Human Decision Making by Increasing Expectations of Volatility.

Smith KE et al. · Jul 1, 2026

People learn most effectively when they can flexibly modify strategies to accommodate environmental changes. Here, we explore how chronic early life stress influences the ways individuals weight and prioritize new information when making decisions. To do so, we examined the choices of 11-16-year-old children in a reward learning task. Children varied on their level of stress exposure. We used a Bayesian computational learning model to assess whether differences in children's decision making were driven by difference in their expectations about the task environment. Children with high stress exposure switched their responses rather than maintaining choices that had previously been effective for them when making decisions about rewards. This switching was driven by children with high stress exposure expecting environments to be more volatile. These findings offer insight into how early life experiences can shape the subsequent parameters of human learning. SUMMARY: How experience shapes an individual's ability to flexibly adjust learning strategies when making decisions is not well understood. Using behavioral tasks combined with a novel computational model, we find exposure to high stress environments biases children towards learning strategies optimal to unpredictable environments. Stress in childhood shapes the development of learning parameters in ways that have implications for decision making.

Neuroscience

Ovarian hormones and high-fat diet duration distinctively modulate hypothalamic chemokine profile.

Augusto AGB et al. · Jul 1, 2026

Excessive intake of saturated fats triggers inflammation in the hypothalamus, a key regulator of energy balance. In the chronic phase of this inflammatory response, bone marrow-derived and lymphoid cells are chemoattracted to this region, partially mitigating high-fat diet (HFD)-induced metabolic impairments. In rodents, the onset and magnitude of this inflammation differ between males and females, reflecting sex-specific patterns of metabolic regulation. However, how the hypothalamic chemokine profile evolves during HFD-induced inflammation, and whether it is influenced by biological sex, remains unclear. Here, male and female C57BL/6J mice were fed a HFD for 1, 3, 14, or 28 days. To isolate the role of ovarian hormones in modulating hypothalamic chemokine profile, we also analyzed ovariectomized (OVX) females with or without estrogen replacement. Quantitative polymerase chain reaction-based expression analysis revealed that most chemokines and their receptors were transiently modulated in the hypothalamus during the course of the HFD exposure, showing reduced levels in the acute phase and normalization during the chronic phase. Despite the modest sex-dependent effects observed, messenger RNA expression of the chemokine receptor C-X-C motif chemokine receptor 3 (CXCR3) was significantly higher in females than in males after 14 and 28 days of HFD, suggesting faster recruitment of CXCR3 + immune cells that may contribute to female protection against metabolic dysfunction. Females lacking ovarian hormone production displayed increased hypothalamic expression of Cxcr3 and Ccl2. Only Cxcr3 expression was partially normalized by estradiol treatment, suggesting that non-estrogenic ovarian factors may play a role in modulating specific chemokine signaling pathways. Together, our findings show that hypothalamic chemokine signaling is dynamically and transiently regulated throughout the phases of HFD-induced inflammation, with Cxcr3 modulation by HFD and ovarian hormones contributing to sex-specific resilience against metabolic inflammation.

Neuroscience

α7nAChR agonist GTS-21 ameliorates sepsis-induced acute kidney injury via MEF2/PGC-1α/HO-1 axis in mice.

Tang YJ et al. · Jul 1, 2026

Background Sepsis-induced acute kidney injury (S-AKI) is a major global public health concern, yet effective therapeutic strategies remain limited. Mitochondrial dysfunction in renal tissues is a key pathogenic mechanism underlying S-AKI. GTS-21, a selective α7 nicotinic acetylcholine receptor (α7nAChR) agonist, exhibits anti-inflammatory and renoprotective effects in S-AKI. Methods We investigated the role of α7nAChR in S-AKI using both in vitro (lipopolysaccharide (LPS)-induced renal tubular cell injury) and in vivo (caecal ligation and puncture (CLP)-induced septic mice) models, with GTS-21 treatment. Results GTS-21 significantly attenuated mitochondrial dysfunction, suppressed apoptosis, and alleviated inflammation, thereby protecting renal tubular cells and renal tissues against LPS- and CLP-induced injury. Mechanistically, GTS-21 activated α7nAChR and upregulated myocyte enhancer factor 2 (MEF2), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and heme oxygenase-1 (HO-1), which collectively mediate its anti-oxidative, anti-apoptotic and anti-inflammatory effects. Conclusion These findings suggest that GTS-21 may represent a potential therapeutic strategy for sepsis-induced kidney injury.

Neuroscience

Circadian-Related Serotonin/Melatonin Level Modulates Cisplatin Ototoxicity Susceptibility Depended on NOS3-NO Pathway.

Qiu S et al. · Jul 1, 2026

Hearing impairment is attributed to factors such as age, genetic predisposition, and environmental influences, among which environmental factors are considered modifiable. Among various environmental factors, the role of poor lifestyle habits is particularly critical, yet the specific mechanisms by which they contribute to hearing damage remain unclear. This study reveals that dysregulated hormone levels due to disrupted light exposure may significantly increase susceptibility to sensorineural hearing loss. In mice, circadian rhythm disruption was found to reduce melatonin and elevate serotonin levels in the inner ear, thereby increasing vulnerability to cisplatin-induced ototoxicity. In both in vivo and in vitro cisplatin-treatment models, we showed that combined treatment with melatonin protected hearing, reduced inner ear cell death, and preserved synaptic connections, whereas serotonin co-administration exacerbated the damage. Using small molecule-protein interaction prediction, we identified NOS3 as a potential target of both melatonin and serotonin, through which they appear to regulate the NO signaling pathway and influence hair cell ferroptosis. Finally, exogenous supplementation of NOS3 in cochlear tissues effectively mitigated cisplatin-induced hair cell damage, even under conditions of circadian rhythm disruption. These findings indicate that the melatonin/serotonin balance modulates susceptibility to sensorineural hearing loss via the NOS3-NO signaling pathway.

Neuroscience