NeuroSci最新文献

Background: Photobiomodulation (PBM), also referred to as low-level light therapy (LLLT), is an emerging non-pharmacological approach. This treatment is considered low-risk, cost-effective, and non-invasive, utilizing near-infrared light (NIR). The purpose of this paper is to explore the underlying mechanism of action and conduct a systematic review of pre-clinical and clinical research on the use of PBM for psychiatric disorders.

Methods: A search on the PubMed, Cochrane Library, and EMBASE databases was performed on 18 and 26 January 2024. Publications focused on PBM treatment in psychiatric disorders such as major depressive disorder, general anxiety disorder, dementia, Parkinson's disease, traumatic brain injury, schizophrenia, and sexual disfunctions were included (n = 23).

Results: Near-infrared stimulation is presented as an effective method, comparable to psychopharmacological treatment. The primary suggested mechanism for PBM is the stimulation of mitochondrial metabolism following the absorption of NIR energy by cytochrome C oxidase. Because of the method of implementation, which omits the liver metabolism of cytochrome P450, PMB is recognized as safe as it does not interact with other drugs.

Limitations: Clinical studies vary in terms of population and treatment parameters, and most do not include a suitable control group.

Conclusions: Preliminary results support the potential of NIR stimulation as a novel and innovative treatment for psychiatry. Further studies are needed to estimate the proper protocols of parameters singly for any disease.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder that affects over 2% of the population worldwide and is characterized by repetitive behaviors, restricted areas of interest, deficits in social communication, and high levels of anxiety. Currently, there are no known effective treatments for the core features of ASD. The previous literature has established erythropoietin (EPO) as a promising antidepressant, working as a potent neurogenic and neurotrophic agent with hematopoietic side effects. Carbamoylated erythropoietin (CEPO), a chemically engineered non-hematopoietic derivative of EPO, appears to retain the neuroprotective factors of EPO without the hematologic properties. Recent evidence shows that CEPO corrects stress-related depressive behaviors in BALB/cJ (BALB) mice, which also have face validity as an ASD mouse model. We investigated whether CEPO can recover deficient social and anxiety-related behavioral deficits compared to C57BL/6J controls. After administering CEPO (40 μg/kg in phosphate-buffered saline) or vehicle over 21 days, we analyzed the mice's performance in the three-chamber social approach, the open field, the elevated plus maze, and the Porsolt's forced swim tasks. CEPO appeared to correct sociability in the three-chamber social approach task to C57 levels, increasing the amount of time the mice interacted with novel, social mice overall rather than altering the overall amount of exploratory activity in the maze. Consistent with this finding, there was no concomitant increase in the distance traveled in the open field, nor were there any alterations in the anxiety-related measures in the task. On the other hand, CEPO administration improved exploratory behavior in the elevated plus maze. This study marks the first demonstration of the benefits of a non-erythropoietic EPO derivative for social behavior in a mouse model of autism and merits further investigation into the mechanisms by which this action occurs.

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the selective loss of dopaminergic (DA) neurons in the midbrain. While dopamine precursor levodopa and D2 receptor agonists are commonly used to alleviate PD symptoms, these treatments do not halt or reverse disease progression. Thus, developing effective neuroprotective strategies remains a critical goal. In this study, we explored neuroprotective mechanisms in a Drosophila primary neuronal culture model of PD, created by administering the environmental toxin rotenone. Using the chemogenetic DREADD (designer receptors exclusively activated by designer drugs) system, we selectively activated cAMP signaling in DA neurons within the rotenone-induced model. Our results demonstrate that increasing cAMP signaling via Gs-coupled DREADD (rM3Ds) is protective against DA neurodegeneration. Furthermore, overexpression of the catalytic PKA-C1 subunit fully rescued DA neurons from rotenone-induced degeneration, with this effect restricted to DA neurons where PKA-C1 was specifically overexpressed. These findings reveal that cAMP-PKA signaling activation is neuroprotective in DA neurons against rotenone-induced degeneration, offering promising insights for developing targeted therapeutic strategies to slow or prevent PD pathology progression.

In recent years, in the pathogenesis of multiple sclerosis, emphasis has been placed on mitochondrial processes that influence the onset of the disease. Oxidative stress would be one of the consequences of mitochondrial dysfunction, and its impact on brain tissue is well described. Microglia, as a brain macrophage, have an important function in removing unwanted metabolites, as well as iron, which is an amplifier of oxidative stress. There are novelties in terms of the connection between these processes, which have redirected research more towards the process of neurodegeneration itself, so that the emphasis is no longer on neuroinflammation, which would initiate the pathological process itself and still exist in the vicinity of lesions with reduced intensity. The aim of this review is to summarize the current knowledge from the literature regarding oxidative stress, mitochondrial dysfunction and iron metabolism and how microglia are involved in these processes in multiple sclerosis.

Environmental noise has been repeatedly linked to negative effects on cognitive functioning among children and adolescents. This research sought to systematically assess studies investigating the relationship between noise exposure and cognitive outcomes in young individuals. Through a meta-analysis of eight primary studies published between 2001 and 2023, this study examined the effects of various noise types on cognitive performance across multiple domains in young populations. The findings reveal that noise exposure significantly impairs cognitive performance in children and adolescents, with a standardized mean difference (SMD) of -0.544 (95% CI: [-0.616, -0.472]), z = -14.85, p < 0.0001. These results underscore the profound impact of environmental noise on cognitive functioning in younger populations.

Background: Stroke and traumatic brain injury (TBI) represent two major health concerns worldwide. There is growing evidence suggesting a potential association between TBI and stroke. In this systematic review and meta-analysis, we aim to explore the association between TBI and stroke risk, with a specific focus on overall stroke risk and subgroup variations based on stroke type, severity, and the post-TBI time period.

Methods: PubMed, Web of Science (WOS), Scopus, and Cochrane Library were systematically searched for studies exploring the link between stroke and TBI. The pooled hazard ratios (HRs) with a 95% confidence interval (CI) were calculated. The Comprehensive Meta-Analysis (CMA) software was used for the analysis. Subgroup analyses were conducted based on stroke type, TBI severity, and post-TBI phase. The Newcastle-Ottawa Scale (NOS) was utilized for the quality assessment.

Results: We included a total of 13 observational studies, with data from 8 studies used for quantitative analysis. A history of TBI was associated with a significantly higher odds of stroke compared to controls (HR = 2.3, 95% CI (1.79 to 2.958), p < 0.001). The risk was greater for hemorrhagic stroke (HR = 4.8, 95% CI (3.336 to 6.942), p < 0.001) than for ischemic stroke (HR = 1.56, 95% CI (1.28 to 1.9), p < 0.001). Both moderate-to-severe TBI (HR = 3.64, 95% CI (2.158 to 6.142), p < 0.001) and mild TBI (HR = 1.81, 95% CI (1.17 to 2.8), p = 0.007) were associated with a significantly higher risk of stroke. The risk was also higher in the early post-TBI phase (1-30 days) (HR = 4.155, 95% CI (2.25 to 7.67), p < 0.001) compared to later phases (HR = 1.68, 95% CI (1.089 to 2.59), p = 0.019) from 30 days to 1 year and (HR = 1.87, 95% CI (1.375 to 2.544), p < 0.001) after 1 year.

Conclusions: This systematic review confirms a significant association between TBI and an increased risk of stroke, regardless of TBI severity, type, or timing of stroke. The findings highlight the need for early monitoring and advocating preventive strategies for stroke in patients with a history of TBI.

People with bipolar disorder (BD) present with mood instability resulting from more frequent and intense emotions in response to environmental conditions relative to healthy subjects. The aim of this study was to investigate the time course of emotion regulation strategies, distraction, and reappraisal in euthymic BD patients (i.e., normal mood range) using electroencephalography (EEG). Fourteen BD patients and 13 matched healthy controls took part in an experiment constituting three conditions, i.e., a passive viewing of positive, negative, and neutral pictures, and two regulation conditions, one with a reappraisal strategy and the other with a distraction strategy. Critically, the ERP results indicated that during passive viewing, the Late Positive Potential (LPP) was larger in BD patients compared with healthy controls, but only for neutral pictures. During emotion regulation, LPP amplitude was reduced in distraction conditions compared with viewing ones, especially for negative emotions in both patients and controls. Importantly, LPP was reduced in reappraisal conditions compared with passive viewing in an early time window for negative emotions and in a later time window for positive emotions in controls but not in patients. Our findings showed that the temporal dynamics of emotion regulation by reappraisal are faster for negative than for positive emotions in controls but not in BD patients.

Insufficient sleep and circadian misalignment increase inflammatory agents. This triggers neuroinflammation and can result in health issues including depression, dementia, lifestyle-related diseases, and industrial accidents. Lactoferrin (LF) confers neuroprotective effects, which are derived from its anti-inflammatory, antioxidant, and iron metabolic properties; however, its roles in acute neuroinflammation and circadian rhythm disruption are yet to be elucidated. Therefore, we aimed to test the effects of LF on rat neuroinflammation and sleep and jetlag in humans. Rats received 7 days of an oral liposomal bovine LF (L-bLF) or vehicle followed by polyriboinosinic:polyribocytidylic acid (poly I:C) peritoneal injections (n = 5-6). Compared with the rats given poly I:C only, the rats given L-bLF and poly I:C had lower Il1b, Tnf, Casp1, Nfe212, Gclm, and Sod2 expression in the hippocampus. This open-label pilot study was carried out on tour conductors performing regular international tour responsibilities, and the data were compared between the initial tour without L-bLF intake and the subsequent tour with L-bLF intake. In the tour with L-bLF intake, L-bLF administration started from one week before the trip and was continued during the trip. In both periods, the tour conductors experienced limited sleep; however, both subjective and objective sleep quality was significantly better with the oral L-bLF intake than without. Overall, we found that prophylactic L-bLF supplementation reduced neuroinflammation in rat hippocampi and improved sleep quality and jetlag in tour conductors.

(1) Background: Multiple lumbar spinal stenosis (LSS) is a degenerative disease that is increasingly prevalent with global aging. Multilevel fusion surgery is burdensome to perform in elderly patients, especially with osteoporosis and underlying disease. This study introduces open midline decompression (OMD) with ligament reconstruction as an alternative stabilization technique for elderly patients with multilevel LSS. (2) Methods: A retrospective review included 42 elderly patients aged 70 or older diagnosed with LSS at three or more levels and who underwent OMD with ligament reconstruction. Pre- and postoperative clinical and radiologic data were analyzed. (3) Results: Thirty-three patients underwent three-level surgeries, and twelve patients underwent four-level surgeries. The mean operative time was 240 ± 42.2 min (74.6 ± 14.9 min per level) with a mean blood loss of 282.9 ± 167.1 cc. Clinical outcome (VAS) and quality of life parameters (SF-12) showed significant improvement after surgery. Postoperative MRI showed sufficient decompression. Dynamic X-rays showed improvement in instability after surgery, but it was statistically insignificant. (4) Conclusions: OMD with ligament reconstruction provides effective neural decompression while preserving the posterior arch and offers soft stabilization with artificial ligaments. It is a safe and viable surgical option for elderly patients with multilevel LSS.

Background: Amputation poses significant physical, psychological, and emotional challenges, with chronic pain being one of the most debilitating outcomes. Pain Pressure Threshold (PPT), a measure of nociceptive sensitivity, is a valuable tool for assessing changes in pain perception. Understanding PPT modulation in amputees is crucial for uncovering the mechanisms underlying pain and developing targeted interventions for pain management.

Objective: This study aimed to evaluate PPT in amputees and identify factors associated with PPT variation in this population.

Methods: This cross-sectional study analyzed neurophysiological, clinical, and demographic data from 86 amputee patients. PPT was assessed as the primary outcome, and its associations with demographic and clinical predictors were examined using both linear and quadratic regression models.

Results: Multivariate analysis identified a significant association between PPT and biological sex, with females exhibiting lower PPT values than males. Quadratic regression analyses revealed inverted U-shaped associations between PPT and age, BMI, and duration since amputation. PPT increased with age, peaking at 45.8 years, followed by a decline. Similar patterns were observed for BMI, peaking at 27.0 kg/m², and for amputation duration, peaking at 26.6 months.

Conclusions: Our findings indicate that sex, age, BMI, and time since amputation are significant factors influencing PPT in amputees, with nonlinear relationships observed for age, BMI, and amputation duration. These results suggest that physiological and disease-related factors (such as age, BMI, and duration of injury) have specific peaks for optimal PPT, highlighting their role in the brain's compensatory system and potential implications for targeted pain management strategies.