AIMS Neuroscience最新文献

Background: The beneficial effects of gardening as a form of physical activity have garnered growing interest in recent years. Existing research suggests that physical activity enhances brain function through modifying synaptic plasticity, growth factor synthesis, and neurogenesis. Gardening physical activity is a promising, cost-effective, non-invasive intervention that can easily be augmented in the rehabilitation of neurodegenerative conditions. However, there is still insufficient literature. This protocol describes a systematic review to be conducted of scientific literature on the benefits of gardening as a physical activity that can promote neuroplasticity and improve cognitive function. This information can be useful as an intervention for persons who experience cognitive impairment brought on by cancer and chemotherapy in developing countries such as South Africa where there is real need to access cognitive rehabilitation.

Methods and analysis: The systematic review strategy will be conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. An electronic literature database search of MEDLINE (PubMed), Embase, Scopus, Cochrane Central Register of Controlled Trials (CENTRAL), and Web of Science will be carried out using medical search terms (MeSH), with English as the only permitted language, during the time period of January 2010 to December 2022. We will search for and review studies on how gardening as a physical activity impacts neuroplasticity and cognition. Two reviewers will read the titles, and abstracts and full text of the studies identified during the search to exclude records that do not meet the inclusion criteria. Data will then be extracted from the remaining studies. Any differences in opinion arising between the reviewers during the procedure will be resolved through discussion with a third reviewer. The Joanna Briggs Institute (JBI) Critical Appraisal Tool checklist will be utilized independently by two reviewers to evaluate the possibility of bias. The included articles will be subjected to narrative synthesis, with the results being presented in a thematic manner.

Ethics and dissemination: There are no need for ethical approval because no patient data will be gathered. The results will be disseminated through an open-access peer-reviewed indexed journal, presented scientific meetings.PROSPERO registration number: CRD42023394493.

Aim: Synthetic MRI (SyMRI) works on the MDME sequence, which acquires the relaxation properties of the brain and helps to measure the accurate tissue properties in 6 minutes. The aim of this study was to evaluate the synthetic MRI (SyMRI)-generated myelin (MyC) to white matter (WM) ratio, the WM fraction (WMF), MyC partial maps performing normative brain volumetry to investigate MyC loss in multiple sclerosis (MS) patients with white-matter hyperintensites (WMHs) and non-MS patients with WMHs in a clinical setting.

Materials and methods: Synthetic MRI images were acquired from 15 patients with MS, and from 15 non-MS patients on a 3T MRI scanner (Discovery MR750w; GE Healthcare; Milwaukee, USA) using MAGiC, a customized version of SyntheticMR's SyMRI® IMAGE software marketed by GE Healthcare under a license agreement. Fast multi-delay multi-echo acquisition was performed with a 2D axial pulse sequence with different combinations of echo time (TEs) and saturation delay times. The total image acquisition time was 6 minutes. SyMRI image analysis was done using SyMRI software (SyMRI Version: 11.3.6; Synthetic MR, Linköping, Sweden). SyMRI data were used to generate the MyC partial maps and WMFs to quantify the signal intensities of test group and control group, andcontrol group , and their mean values were recorded. All patients also underwent conventional diffusion-weighted imaging, i.e., T1w and T2w imaging.

Results: The results showed that the WMF was significantly lower in the test group than in the control group (38.8% vs 33.2%, p < 0.001). The Mann-Whitney U nonparametric t-test revealed a significant difference in the mean myelin volume between the test group and the control group (158.66 ± 32.31 vs. 138.29 ± 29.28, p = 0.044). Also, there were no significant differences in the gray matter fraction and intracranial volume between the test group and the control group.

Conclusions: We observed MyC loss in test group using quantitative SyMRI. Thus, myelin loss in MS patients can be quantitatively evaluated using SyMRI.

Neuropeptide S (NPS), which is a peptide that is involved in the regulation of the stress response, seems to be relevant to the mechanism of action of antidepressants that have anxiolytic properties. However, to date, there have been no reports regarding the effect of long-term treatment with escitalopram or venlafaxine on the NPS system under stress conditions. This study aimed to investigate the effects of the above-mentioned antidepressants on the NPS system in adult male Wistar rats that were exposed to neonatal maternal separation (MS). Animals were exposed to MS for 360 min. on postnatal days (PNDs) 2-15. MS causes long-lasting behavioral, endocrine and neurochemical consequences that mimic anxiety- and depression-related features. MS and non-stressed rats were given escitalopram or venlafaxine (10mg/kg) IP from PND 69 to 89. The NPS system was analyzed in the brainstem, hypothalamus, amygdala and anterior olfactory nucleus using quantitative RT-PCR and immunohistochemical methods. The NPS system was vulnerable to MS in the brainstem and amygdala. In the brainstem, escitalopram down-regulated NPS and NPS mRNA in the MS rats and induced a tendency to reduce the number of NPS-positive cells in the peri-locus coeruleus. In the MS rats, venlafaxine insignificantly decreased the NPSR mRNA levels in the amygdala and a number of NPSR cells in the basolateral amygdala, and increased the NPS mRNA levels in the hypothalamus. Our data show that the studied antidepressants affect the NPS system differently and preliminarily suggest that the NPS system might partially mediate the pharmacological effects that are induced by these drugs.

Patients with lesions in the posterior cingulate gyrus (PCG), including the retrosplenial cortex (RSC) and posterior cingulate cortex (PCC), cannot navigate in familiar environments, nor draw routes on a 2D map of the familiar environments. This suggests that the topographical knowledge of the environments (i.e., cognitive map) to find the right route to a goal is represented in the PCG, and the patients lack such knowledge. However, theoretical backgrounds in neuronal levels for these symptoms in primates are unclear. Recent behavioral studies suggest that human spatial knowledge is constructed based on a labeled graph that consists of topological connections (edges) between places (nodes), where local metric information, such as distances between nodes (edge weights) and angles between edges (node labels), are incorporated. We hypothesize that the population neural activity in the PCG may represent such knowledge based on a labeled graph to encode routes in both 3D environments and 2D maps. Since no previous data are available to test the hypothesis, we recorded PCG neuronal activity from a monkey during performance of virtual navigation and map drawing-like tasks. The results indicated that most PCG neurons responded differentially to spatial parameters of the environments, including the place, head direction, and reward delivery at specific reward areas. The labeled graph-based analyses of the data suggest that the population activity of the PCG neurons represents the distance traveled, locations, movement direction, and navigation routes in the 3D and 2D virtual environments. These results support the hypothesis and provide a neuronal basis for the labeled graph-based representation of a familiar environment, consistent with PCG functions inferred from the human clinicopathological studies.

Obesity represents one of the wellness diseases concurring to increase the incidence of diabetes, cardiovascular diseases, and cancer. One of the main perpetuating factors of obesity is food craving, which is characterized by an urgent desire to eat a large and various amount of food, regardless of calories requirement or satiety signals, and it might be addressed to the alteration of the dorsolateral prefrontal cortex (DLPFC) activity. Despite most of the gold-standard therapies focus on symptom treatment only, non-invasive brain stimulation techniques such as transcranial direct current stimulation (tDCS) could help treat overeating by modulating specific neural pathways. The current systematic review was conducted to identify whether convergent evidence supporting the usefulness of tDCS to deal with food craving are present in the literature. The review was conducted by searching articles published up to January 1^st 2022 on MEDLINE, Scopus and PsycInfo databases. We included studies investigating the effects of tDCS on food craving in subjects affected by overweight and obesity. According to eligibility criteria, 5 articles were included. Results showed that tDCS targeting left DLPFC with unipolar montage induced ameliorating effects on food craving. Controversial results were shown for the other studies, that might be ascribable to the use of bipolar montage, and the choice of other target areas. Further investigations including expectancy effect control, larger sample sizes and follow-up are needed to support more robust conclusions. To conclude, tDCS combined with the use of psychoeducative intervention, diet and physical activity, might represents a potential to manage food craving in individuals with overweight and obesity.

According to the World Health Organization (WHO), traumatic brain injury (TBI) will mainly contribute to disability and death by 2020. Facial fractures associated with TBI are a significant public health concern worldwide. The main etiological factors are road traffic accidents, violence, and falls. Neurological injury associated with facial fractures has been reported to be as high as 76%. Therefore, we retrospectively evaluated facial fracture patterns in patients with a traumatic brain injury in Hospital Universiti Sains Malaysia and evaluated their associations in our study. Ordinal regression was used to examine the facial fracture patterns in patients with traumatic brain injuries. The confounding variables were controlled using ordinal regression analysis, and probabilities of p < 0.1 were considered significant associations. The results found that zygomatic arch fracture -1.141 (95% CI, -2.487 to 0.204, p-value = 0.096), Le Fort II fracture -1.080 (95% CI, -2.138 to -0.022, p-value = 0.045), maxillary bone fracture 2.924 (95% CI, 1.784 to 4.063, p-value .001), nasal bone fracture 4.047 (95% CI, 1.243 to 6.851, p-value = 0.005), and mandibular bone fracture 1.501 (95% CI, 0.711 to 2.291, p-value .001) were the most common facial fracture types associated with traumatic brain injury (TBI). This study provides valuable data for creating prevention plans and gives a chance to discover the epidemiology, prevalence, and connection between TBI and facial fracture.