Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent urological disorder characterized by persistent pelvic pain, urinary symptoms, and significant impact on quality of life. In addition to its clinical symptoms, CP/CPPS is frequently associated with psychiatric comorbidities, such as anxiety and depression, indicating complex neurobiological mechanisms. This review explores the mechanisms linking CP/CPPS with affective disorders, emphasizing central nervous system alterations, dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, and neuroimmune interactions. Evidence in-dicates that central sensitization, microglial and astrocytic activation, and elevated proinflammatory cytokines (IL-1β, IL-6, TNF-α) contribute to maladaptive painemotion network interactions. Additionally, dysregulation of hormones and neurotransmitters may exacerbate both pain perception and mood disorders. Psychosocial factors, including stress, coping strategies, and cognitive-emotional processes, further modulate symptom severity and treatment outcomes, highlighting the importance of a biopsychosocial approach. Gaining a deeper understanding of the neurobiological and psychosocial mechanisms behind anxiety and depression in CP/CPPS can lead to more effective, multidimensional management strategies and enhance patient-centered care.

Current standard treatments for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), a urological disorder with anxiety as a major comorbidity, are limited in success rates. Recent findings revealed the anti-inflammatory and neuroprotective effects of CO-releasing molecules (CO-RMs), but there is a gap in the knowledge on its effects in CP/CPPS. Therefore, the objective of our study was to investigate the potential therapeutic effects of CORM-A1 on the scrotal pain threshold and anxiety-related behaviors in experimental model of CP/CPPS. Adult Wistar albino male rats were randomized to Sham (intraprostatic saline) or CP/CPPS (intraprostatic λ-carrageenan) groups (n = 12). Half received CORM-A1 (2 mg/kg/day, i.p., days 1–7), others PBS, forming four subgroups (n = 6). The pain threshold (by an electronic von Frey esthesiometer) and anxiety-like behavior (by an open field, elevated plus maze and light/dark test) were assessed; prostates were histologically examined. Carrageenan-induced CP/CPPS caused significant mechanical pain hypersensitivity (p < 0.001), anxiety-like behaviors (p < 0.001–0.05), and histological prostate damage when compared to corresponding Sham groups. CORM-A1 treatment increased pain thresholds (p < 0.001) and improved behavioral outcomes (p < 0.001–0.01) in all ethological tests. These findings indicate that CORM-A1 exerts analgesic and anxiolytic effects in an experimental model of CP/CPPS in rats.

Background and Objectives: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a complex disease that involves changes in multiple organs and even the central nervous system (CNS). CP/CPPS may elevate seizure risk via neuroinflammatory mechanisms within the CNS. Neuroprotective effects of CO-releasing molecules (CORMs) were demonstrated in inflammation-driven conditions, while CORMs potential to ameliorate seizure susceptibility in inflammatory states, like CP/CPPS, remains unclear. Therefore, we investigated effects of CORM-A1 on susceptibility to lindane–induced seizures in rats with CP/CPPS through behavioral and electroencephalographic (EEG) study. Materials and Methods: Wistar rats were divided into four groups (n = 8/group): Sham-PBS, Sham-CORM, CP/CPPS-PBS and CP/CPPS-CORM. The CP/CPPS model was created by injection of 3% λ-carrageenan and its development assessed by mechanical pain threshold. CORM-A1 (2 mg/kg/day, i.p.) or vehicle (PBS) was given during seven postoperative days. Hereupon, subconvulsive dose of lindane (4 mg/kg, i.p.) was administered and behavioral features of seizures were observed alongside with EEG recordings. Results: Our data showed that the incidence and severity of lindane-induced seizures was significantly higher in the CP/CPPS-PBS group than in the Sham-PBS group. CORM-A1 treatment significantly decreased seizure incidence, prolonged seizure latency, and reduced seizure severity in CP/CPPS rats compared to vehicle treatment (CP/CPPS-CORM vs. CP/CPPS-PBS). Also, CORM-A1 treatment significantly reduced the number and duration of ictal periods induced by lindane in CP/CPPS animals compared to vehicle treatment. Conclusions: It could be concluded that CORM-A1 treatment reduced both behavioral and EEG signs of increased seizure susceptibility in rats with CP/CPPS, thus it could be a potential therapeutic target.

Rising global temperatures and more frequent heat waves pose a growing threat to public health, particularly among older adults. Age-related declines in thermoregulatory capacity such as reduced sweating, impaired vasodilation, and diminished hypothalamic responsiveness make it more difficult to cope with elevated nighttime temperatures. These thermal challenges disrupt sleep by prolonging sleep onset, fragmenting slow-wave and REM sleep, and suppressing melatonin secretion. Importantly, sex-related differences in thermoregulatory aging—particularly menopause-associated vasomotor instability in women and testosterone-related autonomic changes in men—further modulate individual vulnerability to heat-induced sleep disruption. Beyond sleep, heat-induced stress affects metabolic, cardiovascular, and immune systems, promoting insulin resistance, endothelial dysfunction, sympathetic overactivation, and chronic inflammation. Socioeconomic disparities, urban heat island exposure, and differential access to cooling infrastructure function as critical environmental modifiers that amplify biological vulnerability, particularly in disadvantaged older populations. This narrative review aims to synthesize current knowledge on the specific thermoregulatory mechanisms of sleep disruption induced by heat stress in older adults. Understanding these interactions is crucial for developing effective interventions, including environmental cooling, circadian-aligned behaviors, and targeted public health strategies, to mitigate the compounded risks of heat exposure and preserve healthy sleep in aging populations. However, many proposed mechanistic pathways are primarily derived from animal models, and controlled human studies specifically targeting heat-exposed older adults remain scarce.

Heatwaves and tropical nights are emerging as significant public health challenges under accelerating climate change, with middle-aged and older adults demonstrating heightened vulnerability. This scoping review maps the existing evidence on how nocturnal heat affects sleep in middle-aged and older adults aged 45 and above, synthesizing findings from experimental and observational studies published in English over the past decade. A comprehensive search of PubMed and Scopus, supplemented by reference screening, identified 31 relevant studies. Data on study design, population characteristics, heat exposure metrics, sleep outcomes, and interventions were charted and synthesized narratively due to methodological heterogeneity. Across studies, elevated nighttime temperatures consistently reduced total sleep time and sleep efficiency, increased wake after sleep onset, and disrupted sleep architecture, particularly REM and N3 stages. Environmental, behavioral, and physiological interventions such as improved ventilation, targeted cooling strategies, and pre-sleep thermal management partially mitigated heat-related sleep disruption. Overall, the findings highlight gaps in standardized exposure metrics and harmonized sleep assessment, providing guidance for future research and public health strategies aimed at protecting sleep health in middle-aged and aging populations amid increasingly frequent extreme heat events.

Wi-Fi is a common source of radiofrequency electromagnetic field (RF-EMF) exposure, operating at 2.4 GHz and 5 GHz frequencies. Increasing experimental evidence suggests that RF-EMF exposure during prenatal and early postnatal periods may influence neurodevelopment and behavior. This review examines the effects of RF-EMF exposure on learning, memory, anxiety-like behaviors, motor activity, and exploratory behaviors. The study is based on 65 experimental studies identified through a literature search conducted in PubMed, Web of Science, and Scopus databases. Mechanistic studies indicate that these effects are associated with increased oxidative stress, impaired synaptic plasticity, and modulation of neuronal signaling pathways, potentially affecting neurogenesis, dendritic spine formation, and the maturation of neural circuits. Findings from animal studies are heterogeneous; while some studies report mild cognitive and motor impairments, others do not observe significant behavioral changes. Human data remain limited and controversial, providing low-level evidence regarding cognitive and behavioral effects. Nevertheless, the sensitivity of the developing nervous system to such exposures is noteworthy. Current evidence suggests that RF-EMF exposure may affect neurodevelopment and behavior through neurobiological mechanisms. However, further standardized, long-term, and multidimensional studies are required to reach definitive conclusions regarding the direction and magnitude of these effects. Factors such as exposure duration, intensity, developmental stage, and sex appear to play critical roles.