AIMS Neuroscience最新文献

Background: Dementia is a prevalent, progressive, neurodegenerative condition with multifactorial causes. Due to the lack of effective pharmaceutical treatments for dementia, there are growing clinical and research interests in using vagus nerve stimulation (VNS) as a potential non-pharmacological therapy for dementia. However, the extent of the research volume and nature into the effects of VNS on dementia is not well understood. This study aimed to examine the extent and nature of research activities in relation to the use of VNS in dementia and disseminate research findings for the potential utility in dementia care.

Methods: We performed a scoping review of literature searches in PubMed, HINARI, Google Scholar, and the Cochrane databases from 1980 to November 30th, 2023, including the reference lists of the identified studies. The following search terms were utilized: brain stimulation, dementia, Alzheimer's disease, vagal stimulation, memory loss, Deme*, cognit*, VNS, and Cranial nerve stimulation. The included studies met the following conditions: primary research articles pertaining to both humans and animals for both longitudinal and cross-sectional study designs and published in English from January 1st, 1980, to November 30th, 2023; investigated VNS in either dementia or cognitive impairment; and were not case studies, conference proceedings/abstracts, commentaries, or ordinary review papers.

Findings and conclusions: We identified 8062 articles, and after screening for eligibility (sequentially by titles, abstracts and full text reading, and duplicate removal), 10 studies were included in the review. All the studies included in this literature review were conducted over the last three decades in high-income geographical regions (i.e., Europe, the United States, the United Kingdom, and China), with the majority of them (7/10) being performed in humans. The main reported outcomes of VNS in the dementia cases were enhanced cognitive functions, an increased functional connectivity of various brain regions involved in learning and memory, microglial structural modifications from neurodestructive to neuroprotective configurations, a reduction of cerebral spinal fluid tau-proteins, and significant evoked brain tissue potentials that could be utilized to diagnose neurodegenerative disorders. The study outcomes highlight the potential for VNS to be used as a non-pharmacological therapy for cognitive impairment in dementia-related diseases such as Alzheimer's disease.

Parkinson's disease (PD) is characterized by the pathological accumulation of α-synuclein, which has driven extensive research into the role of exosomes in disease mechanisms. Exosomes are nanoscale vesicles enriched with proteins, RNA, and lipids that facilitate critical intercellular communication processes. Recent studies have elucidated the role of exosomes in transmitting misfolded proteins among neurons, which significantly impacts the progression of PD. The presence of disease-associated exosomes in cerebrospinal fluid and blood highlights their substantial diagnostic potential for PD. Specifically, exosomes derived from the central nervous system (CNS) have emerged as promising biomarkers because of their ability to accurately reflect pathological states. Furthermore, the isolation of exosomes from distinct brain cell types allows the identification of precise biomarkers, increasing diagnostic specificity and accuracy. In addition to being useful for diagnostics, exosomes hold therapeutic promise given their ability to cross the blood-brain barrier (BBB) and selectively modulate their cargo. These findings suggest that these materials could be used as delivery systems for therapeutic drugs for the treatment of neurodegenerative diseases. This review comprehensively examines the multifaceted roles of exosomes in PD pathogenesis, diagnosis, and treatment. It also addresses the associated clinical challenges and underscores the urgent need for further research and development to fully leverage exosome-based strategies in PD management.

Embodiment (the sensation that arises when the properties of an external instrument are processed as if they are the attributes of one's own biological body) and (tele)presence (the sensation of being fully engaged and immersed in a location other than the physical space occupied by one's body) sustain the perception of the physical self and potentially improve performance in teleoperations (a system that enables human intelligence to control robots and requires implementing an effective human-machine interface). Embodiment and presence may be interdependent and influenced by right temporo-parietal junction (rTPJ) activity. We investigated the interplay between embodiment, (tele)presence, and performance in teleoperation, focusing on the role of the rTPJ. Participants underwent a virtual reality task with transcranial direct current stimulation (tDCS) twice, receiving either active or sham stimulation. Behavioral measures (driving inaccuracy, elapsed time in the lap, time spent in attentional lapses, short-term self-similarity, and long-term self-similarity), perceived workload (mental demand, physical demand, temporal demand, own performance, effort, and frustration), embodiment's components (ownership, agency, tactile sensations, location, and external appearance), and presence's components (realism, possibility to act, quality of interface, possibility to examine, self-evaluation of performance, haptic, and sounds) were assessed. The results showed that rTPJ stimulation decreased perceived ownership but enhanced presence with changes in the complexity of visuomotor adjustments (long and short-term self-similarity indices). Structural equation modeling revealed that embodiment increased visuomotor inaccuracy (a composite variable of overall performance, including deviations from the optimal trajectory and the time taken to complete the task), presence reduced workload, and workload increased inaccuracy. These results suggested a dissociation between embodiment and presence, with embodiment hindering performance. Prioritizing virtual integration may lower human performance, while reduced workload from presence could aid engagement. These findings emphasize the intricate interplay between rTPJ, subjective experiences, and performance in teleoperation.

Background: Schizophrenia is characterized by significant cognitive impairments and affects up to 98% of patients. Neurofeedback (NF) offers a means to modulate neural network function through cognitive processes such as learning and memorization, with documented structural changes in the brain, most notably an increase in grey matter volume in targeted regions.

Methods: The present 2-week, open-label, preliminary study aims to evaluate the efficacy on cognition of an adjunctive short and intensive (8 daily sessions lasting 30 minutes) alpha/theta NF training in a sample of subjects affected by schizophrenia on stabilized treatment with atypical antipsychotic drugs. The efficacy was measured at baseline and at the end of the study by the Brief Neuropsychological Examination 2 (ENB 2), the Mini Mental State Examination (MMSE), and the Stroop color-word interference test; the clinical symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS).

Results: A final sample of nine patients completed the study. Regarding the cognitive performance, at the final assessment (week 2), the NF treatment significantly improved the performance in the "Story Recall Immediate" (p = 0.024), "Story Recall Delayed" (p = 0.007), "Interference Memory 30 s" (p = 0.024), "Clock Test" (p = 0.014) sub-tests, and the ENB2 Total Score (p = 0.007). Concerning the clinical symptoms, no significant changes were observed in the PANSS subscales and the PANSS Total score.

Conclusions: NF could represent an adjunctive treatment strategy in the therapeutic toolbox for schizophrenia cognitive symptoms.

Parkinson's disease (PD) is a neurodegenerative disorder that involves the loss of dopaminergic neurons, which leads to motor and non-motor symptoms that have a significant impact. The pathophysiology of PD is complex and involves environmental and genetic factors that contribute to alpha-synuclein aggregation, mitochondrial dysfunction, oxidative stress, and neuroinflammation. The current treatments of PD primarily focus on symptom management and have limitations in addressing disease progression and non-motor symptoms. Epidemiological data indicates a rise in PD cases worldwide, which highlights the need for effective treatments. Pathophysiological insights point out the involvement of various factors in PD progression, such as dopamine dysregulation, genetic mutations, oxidative stress, mitochondrial damage, alpha-synuclein aggregation, and neuroinflammation. Although current treatments, which include dopamine precursors, monoamine oxidase (MAO) inhibitors, and non-dopaminergic drugs, can alleviate motor symptoms, they are not effective in preventing disease progression or managing non-motor symptoms. Additionally, they can lead to adverse effects and become less effective over time. Novel therapeutic approaches, including cell-based therapies, gene therapies, targeted drug delivery therapies, and magnetic field therapies, are promising in improving symptom management and providing personalized treatment. Additionally, emerging therapies that target alpha-synuclein aggregation, mitochondrial dysfunction, and neuroinflammation may have potential disease-modifying effects. To sum up, for dealing with the multiple aspects of PD, there is a great need to come up with new and creative therapeutic approaches that not only relieve symptoms, but also prevent the progression of disease and non-motor symptoms. The progress made in comprehending the underlying mechanisms of PD provides optimism for developing successful treatments that can enhance the outcomes and quality of life.

The study of the brain-gut axis and its impact on cognitive function and in the development of neurodegenerative diseases is a very timely topic of interest to researchers. This review summarizes information on the basic mechanisms of gut-brain communication. We then discuss the roles of the gut microbiome as a neuroprotective factor in neurodegeneration. The gut microbiota is extremely important in maintaining the body's homeostasis, shaping the human immune system and the proper functioning of the brain. The intestinal microflora affects the processes of neuroplasticity, synaptogenesis, and neuronal regeneration. This review aims to explain changes in the composition of the bacterial population of the intestinal microflora among patients with Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Abnormalities in gut microflora composition are also noted in stress, depression, or autism spectrum development. New observations on psychobiotic supplementation in alleviating the symptoms of neurodegenerative diseases are also presented.

Intracellular potassium ion (K⁺) concentration is higher than extracellular K⁺ concentration. Some cells maintain intracellular potassium levels by taking up extracellular potassium. However, investigating these details requires techniques to measure intracellular potassium concentrations. We established a method to easily measure intracellular potassium concentrations using a simpler electrode. The LAQUAtwin K-11 was capable of linearly quantifying potassium concentrations and was not affected by cellular constituents other than nucleic acids; however, it did not tolerate low temperatures. Interference caused by a high concentration of nucleic acids was eliminated by the addition of cations. It was also suggested that the concentration of nucleic acids in the cell suspension was not sufficiently high to interfere with the measurements. Intracellular potassium concentrations increased and decreased in response to extracellular potassium concentrations. Exposure to valinomycin did not decrease the potassium concentration, suggesting that re-uptake of the potassium released outside the cells occurred immediately. Additionally, potassium concentrations could be measured in the brain tissue homogenates using the device. This measurement method can track the relative changes in potassium concentration in cells under various conditions and in tissues of various disease models.

Purpose: The cyclic AMP response element-binding protein (CREB) and nerve growth factor (NGF) have been proposed as key modulators of brain health and are involved in synaptic plasticity. The study investigates how combined water-based training affects hippocampal neuron plasticity and memory function in old rats.

Methods: 16 Wistar male rats 24-month-old were randomly divided into two groups: combined training (n = 8) and control (n = 8). Four sessions were performed per week for 10 weeks, and consisted of resistance and endurance training in water. The control group was placed in a water container during training for 30 minutes to be homogenized in terms of the stress conditions. The.NGF and CREB genes in the hippocampus were evaluated and the working memory was measured using real-time PCR and Y-maze tests. The SPSS 26 software was utilized in which independent t-tests were used to analyze the genes and the Mann-Whitney U test was used to analyze functional memory with a significant level of (P < 0.05).

Results: The combined training resulted in a significant rise in NGF and CREB gene expression in the hippocampus tissue of elderly rats compared to the control group (P < 0.05); however, there was no notable difference in the Y maze performance test between the two groups (P < 0.05).

Conclusions: These findings suggest that water-based combined training has beneficial effects on gene expression of NGF and CREB; however, it is necessary to conduct more studies to comprehend the effects of combined training on memory function.

Physical activity during the developmental age is an indispensable tool for the physical and mental growth of children. Thanks to physical activity, individuals have the opportunity to improve their physical efficiency and promote better health, establish relationships with the environment and with others, and develop cognitive processes. Therefore, the aim of this study is to investigate the relationship between physical activity and the development of scholastic prerequisites among kindergarten children. 52 children (aged 4-5) participated in either a classroom-based physical activity program (60'/3 days per week) or regular lessons. At the beginning and end of the intervention programs, a set of standardized motor evaluation tests and the Observational Questionnaire for the Early Identification of Learning Disabilities (IPDA) were administered. As a result, a meaningful Time x Group interaction for the IPDA Variable was observed. The aforementioned development denotes a noteworthy advancement within the treatment group (p < 0.001). Conversely, no substantial modification was noted in the control group. The findings derived from this study provide a foundational support to the concept that physical activity integrated into classroom settings is an effective strategy to improve both scholastic prerequisites and academic performance.

Pain is an essential aspect of the body's physiological response to unpleasant noxious stimuli from either external sustained injuries or an internal disease condition that occurs within the body. Generally, pain is temporary. However, in patients with neuropathic pain, the experienced pain is persistent and uncontrollable, with an unsatisfactory treatment effectiveness. The activation of the immune system is a crucial factor in both central and peripheral neuropathic pain. The immune response plays an important role in the progression of the stages of neuropathic pain, and acts not only as pain mediators, but also produce analgesic molecules. Neuropathic pain has long been described as a result of dysfunctional nerve activities. However, there is substantial evidence indicating that the regulation of hyperalgesia is mediated by astrocytes and microglia activation. Mesenchymal stem cells currently hold an optimal potential in managing pain, as they can migrate to damaged tissues and have a robust immunosuppressive role for autologous or heterologous transplantation. Moreover, mesenchymal stem cells revealed their immunomodulatory capabilities by secreting growth factors and cytokines through direct cell interactions. The main idea underlying the use of mesenchymal stem cells in pain management is that these cells can replace damaged nerve cells by releasing neurotrophic factors. This property makes them the perfect option to modulate and treat neuropathic pain, which is notoriously difficult to treat.