AIMS Neuroscience最新文献

Spinal cord injury (SCI) is a debilitating condition that results in impaired sensory and motor function due to the limited self-regenerative ability of the spinal cord. To address this issue, combination therapy has been proposed as an effective treatment strategy for SCI regeneration. In this study, Platelet-Rich Plasma (PRP)-derived exosomes loaded with dexamethasone were utilized in a mouse model of SCI compression. PRP-derived exosomes loaded with dexamethasone (Dex) were prepared using ultracentrifugation and sonication methods and were administered to the mice via intravenous injection. Following a four-week duration, behavioral assessments were administered to assess functional recuperation, and diverse metrics encompassing the expression of genes associated with apoptosis and antiapoptosis, serum cytokine concentrations and tissue sampling were subjected to thorough examination. The results of this study demonstrated that mice treated with PRP-derived exosomes loaded with Dex (ExoDex) exhibited altered levels of TNF-α and IL-10, along with decreased Bax and increased Bcl2 expression in comparison to the model group. Furthermore, intravenously injected ExoDex reduced the size of the lesion site, lymphocyte infiltration, vacuolation, cavity size and tissue disorganization while also improving locomotor recovery. We propose that the utilization of exosome-loaded Dex therapy holds potential as a promising and clinically relevant approach for injured spinal cord repair. However, further extensive research is warranted in this domain to validate and substantiate the outcomes presented in this study.

Errors can affect our memory, yet even when there are gaps in our recollection of events, memory often serves us fairly well. Memory formation involves at least three different sub-processes, that are regulated by an underlying neural structure. From a cognitive neuropsychological perspective, a complex process of encoding, consolidating, and retrieval is involved in remembering an event, and it might be hindered by one's emotional state, physiological response to the event itself, and misinformation. As a result, it is very likely that one may struggle to remember specifics of what happened which can increase our susceptibility to the formation of false memories. This has major implications for everyday functioning, as in the case when you mistakenly remember you took your pills when you never did, or where errors have led to false accusations about trauma or abuse, and wrongful convictions of crimes. Memories sometimes contain biases and inaccuracies that prevent them from accurately recalling events. The review will provide an updated overview of current research advances on the cognitive and neural mechanisms underlying inaccurate, distorted, or false memories.

Multiple sclerosis (MS) is a debilitating autoimmune condition caused by demyelination, neurodegeneration and persistent inflammation of the central nervous system. Pediatric multiple sclerosis (PMS) is a relatively rare form of the disease that affects a significant number of individuals with MS. Environmental exposures, such as viral infections and smoking, can interact with MS-associated human leukocyte antigens (HLA) risk alleles and influence the immune response. Upregulation of immune response results in the disruption of immune balance leading to cascade of inflammatory events. It has also been established that gut microbiome dysbiosis poses a higher risk for pro-inflammation, and it is essentially argued to be the greatest environmental risk factor for MS. Dysbiosis can cause an unusual response from the adaptive immune system and significantly contribute to the development of disease in the host by activating pro-inflammatory pathways that cause immune-mediated disorders such as PMS, rendering the body more vulnerable to foreign attacks due to a weakened immune response. All these dynamic interactions between biological, environmental and genetic factors based on epigenetic study has further revealed that upregulation or downregulation of some genes/enzyme in the central nervous system white matter of MS patients produces a less stable form of myelin basic protein and ultimately leads to the loss of immune tolerance. The diagnostic criteria and treatment options for PMS are constantly evolving, making it crucial to have a better understanding of the disease burden on a global and regional scale. The findings from this review will aid in deepening the understanding of the interplay between genetic and environmental risk factors, as well as the role of the gut microbiome in the development of pediatric multiple sclerosis. As a result, healthcare professionals will be kept abreast of the early diagnostic criteria, accurately delineating other conditions that can mimic pediatric MS and to provide comprehensive care to individuals with PMS based on the knowledge gained from this research.

Parkinson's disease (PD) is a progressive neurodegenerative disorder that affects motor and cognition functions. The etiology of Parkinson's disease remains largely unknown, but genetic and environmental factors are believed to play a role. The neurotransmitter dopamine is implicated in regulating movement, motivation, memory, and other physiological processes. In individuals with Parkinson's disease, the loss of dopaminergic neurons leads to a reduction in dopamine levels, which causes motor impairment and may also contribute to the cognitive deficits observed in some patients. Therefore, it is important to understand the pathophysiology that leads to the loss of dopaminergic neurons, along with reliable biomarkers that may help distinguish PD from other conditions, monitor its progression, or indicate a positive response to a therapeutic intervention. Important advances in the treatment, etiology, and pathogenesis of Parkinson's disease have been made in the past 50 years. Therefore, this review tries to explain the different possible mechanisms behind the depletion of dopamine in PD patients such as alpha-synuclein abnormalities, mitochondrial dysfunction, and 3,4-dihydroxyphenylacetaldehyde (DOPAL) toxicity, along with the current therapies we have and the ones that are in development. The clinical aspect of Parkinson's disease such as the manifestation of both motor and non-motor symptoms, and the differential diagnosis with similar neurodegenerative disease are also discussed.

Human and animal diseases have always been reported to be treated by medicinal herbs owing to their constituents. Excess sodium metavanadate is a potential environmental toxin when consumed and could induce oxidative damage leading to various neurological disorders and Parkinsons-like diseases. This study is designed to investigate the impact of the flavonoid Glycoside Fraction of Ginkgo Biloba Extract (GBE) (at 30 mg/kg body weight) on vanadium-treated rats. Animals were divided randomly into four groups: Control (Ctrl, normal saline), Ginkgo Biloba (GIBI, 30mg/kg BWT), Vanadium (VANA, 10 mg/kg BWT) and Vanadium + Ginkgo biloba (VANA + GIBI). Markers of oxidative stress (Glutathione Peroxidase and Catalase) were assessed and found to be statistically increased with GIBI when compared with CTRL and treatment groups. Results from routine staining revealed that the control and GIBI group had a normal distribution of cells and a pronounced increase in cell count respectively compared to the VANA group. When compared to the VANA group, the NeuN photomicrographs revealed that the levels of GIBI were within the normal range (***p < 0.001; ** p < 001). The treatment with GIBI showed a better response by increasing the neuronal cells in the VANA+GIBI when compared with the VANA group. The NLRP3 Inflammasome photomicrographs denoted that there was a decrease in NLRP3-positive cells in the control and GIBI groups. The treatment group shows fewer cells compared to that of the VANA group. The treatment group shows fewer cells compared to that of the VANA group. The findings of the study confirmed that ginkgo biloba extract via its flavonoid glycoside fraction has favorable impacts in modulating vanadium-induced brain damage with the potential ability to lower antioxidant levels and reduce neuroinflammation.

Procedures for neurological disorders such as Parkinsons Disease (PD), Essential Tremor (ET), Obsessive Compulsive Disorder (OCD), Tourette's Syndrome (TS), and Major Depressive Disorder (MDD) tend to overlap. Common therapeutic procedures include deep brain stimulation (DBS), lesioning, and focused ultrasound (FUS). There has been significant change and innovation regarding targeting mechanisms and new advancements in this field allowing for better clinical outcomes in patients with severe cases of these conditions. In this review, we discuss advancements and recent discoveries regarding these three procedures and how they have led to changes in utilization in certain conditions. We further discuss the advantages and drawbacks of these treatments in certain conditions and the emerging advancements in brain-computer interface (BCI) and its utility as a therapeutic for neurological disorders.

The possibility of multimodality imaging with PET/MR and the availability of ultra-high field MRI has allowed to investigate novel aspects of neuropsychiatric conditions. One of the major barriers in current studies is the lack of an instrument that allows to accurately cover the temporal aspect under the same physiological conditions. The aim of this commentary is to provide our perspective on how the integration of EEG-PET-MR could be a solution to the current challenge in molecular imaging and seems to hold great promise in future pharmacological challenging-based studies, understanding different functional states of the brain, and could furthermore aid in the diagnostic and prognostic evaluations of neurocognitive disorders.

Mild cognitive impairment (MCI) is often considered a precursor to Alzheimer's disease (AD) and early diagnosis may help improve treatment effectiveness. To identify accurate MCI biomarkers, researchers have utilized various neuroscience techniques, with electroencephalography (EEG) being a popular choice due to its low cost and better temporal resolution. In this scoping review, we analyzed 2310 peer-reviewed articles on EEG and MCI between 2012 and 2022 to track the research progress in this field. Our data analysis involved co-occurrence analysis using VOSviewer and a Patterns, Advances, Gaps, Evidence of Practice, and Research Recommendations (PAGER) framework. We found that event-related potentials (ERP), EEG, epilepsy, quantitative EEG (QEEG), and EEG-based machine learning were the primary research themes. The study showed that ERP/EEG, QEEG, and EEG-based machine learning frameworks provide high-accuracy detection of seizure and MCI. These findings identify the main research themes in EEG and MCI and suggest promising avenues for future research in this field.