Abstract:Repetitive transcranial magnetic stimulation has been increasingly studied in different neurological diseases, and although most studies focus on its effects on neuronal cells, the contribution of non-neuronal cells to the improvement triggered by repetitive transcranial magnetic stimulation in these diseases has been increasingly suggested. To systematically review the effects of repetitive magnetic stimulation on non-neuronal cells two online databases, Web of Science and PubMed were searched for the effects… Show more
“…Our findings align with previous studies in healthy rodents, where authors reported no changes in microglia and astrocyte reactivity after 3 and 5 sessions of high and low frequency rTMS stimulation [ 10 , 11 , 65 ]. In contrast, in rat models of spinal cord injury and chronic pain and depression, rTMS decreased microglia activation and inflammatory markers after 8 and 4 weeks of daily rTMS [ 66 , 67 ].…”
Section: Discussionsupporting
confidence: 93%
“…In contrast, in rat models of spinal cord injury and chronic pain and depression, rTMS decreased microglia activation and inflammatory markers after 8 and 4 weeks of daily rTMS [ 66 , 67 ]. This discrepancy might suggest that rTMS modulates microglia activity when it is already in an active state and might have no effects when delivered in healthy subjects, as indicated in a recent literature review [ 65 ]. Alternatively, discrepancy of results might stem from differences in the study design, such as the subject brain size and stimulated areas (non-human primate versus rodent brain size), or the number of stimulation sessions (3 weeks of stimulation delivered in the current study versus the 4 and 8 weeks of delivery by [ 66 , 67 ]).…”
Section: Discussionmentioning
confidence: 99%
“…Current work centered on the evaluation of glial activation as an indirect way to evaluate rTMS safety; however, it is worth noting that previous research has also explored the protective effects of stimulation mediated through glial cells (for a comprehensive review, refer to [ 65 ]). Nonetheless, the number of available studies in this area remains limited and has predominantly been conducted in rodents, thus constraining its applicability to human subjects.…”
While the applicability and popularity of theta burst stimulation (TBS) paradigms remain, current knowledge of their neurobiological effects is still limited, especially with respect to their impact on glial cells and neuroinflammatory processes. We used a multimodal imaging approach to assess the effects of a clinical course of TBS on markers for microglia activation and tissue injury as an indirect assessment of neuroinflammatory processes. Healthy non-human primates received continuous TBS (cTBS), intermittent TBS (iTBS), or sham stimulation over the motor cortex at 90% of resting motor threshold. Stimulation was delivered to the awake subjects 5 times a week for 3–4 weeks. Translocator protein (TSPO) expression was evaluated using Positron Emission Tomography and [11C]PBR28, and myo-inositol (mI) and N-acetyl-aspartate (NAA) concentrations were assessed with Magnetic Resonance Spectroscopy. Animals were then euthanized, and immunofluorescence staining was performed using antibodies against TSPO. Paired t-tests showed no significant changes in [11C]PBR28 measurements after stimulation. Similarly, no significant changes in mI and NAA concentrations were found. Post-mortem TSPO evaluation showed comparable mean immunofluorescence intensity after active TBS and sham delivery. The current study suggests that in healthy brains a clinical course of TBS, as evaluated with in-vivo imaging techniques (PET and MRS), did not measurably modulate the expression of glia related markers and metabolite associated with neural viability.
“…Our findings align with previous studies in healthy rodents, where authors reported no changes in microglia and astrocyte reactivity after 3 and 5 sessions of high and low frequency rTMS stimulation [ 10 , 11 , 65 ]. In contrast, in rat models of spinal cord injury and chronic pain and depression, rTMS decreased microglia activation and inflammatory markers after 8 and 4 weeks of daily rTMS [ 66 , 67 ].…”
Section: Discussionsupporting
confidence: 93%
“…In contrast, in rat models of spinal cord injury and chronic pain and depression, rTMS decreased microglia activation and inflammatory markers after 8 and 4 weeks of daily rTMS [ 66 , 67 ]. This discrepancy might suggest that rTMS modulates microglia activity when it is already in an active state and might have no effects when delivered in healthy subjects, as indicated in a recent literature review [ 65 ]. Alternatively, discrepancy of results might stem from differences in the study design, such as the subject brain size and stimulated areas (non-human primate versus rodent brain size), or the number of stimulation sessions (3 weeks of stimulation delivered in the current study versus the 4 and 8 weeks of delivery by [ 66 , 67 ]).…”
Section: Discussionmentioning
confidence: 99%
“…Current work centered on the evaluation of glial activation as an indirect way to evaluate rTMS safety; however, it is worth noting that previous research has also explored the protective effects of stimulation mediated through glial cells (for a comprehensive review, refer to [ 65 ]). Nonetheless, the number of available studies in this area remains limited and has predominantly been conducted in rodents, thus constraining its applicability to human subjects.…”
While the applicability and popularity of theta burst stimulation (TBS) paradigms remain, current knowledge of their neurobiological effects is still limited, especially with respect to their impact on glial cells and neuroinflammatory processes. We used a multimodal imaging approach to assess the effects of a clinical course of TBS on markers for microglia activation and tissue injury as an indirect assessment of neuroinflammatory processes. Healthy non-human primates received continuous TBS (cTBS), intermittent TBS (iTBS), or sham stimulation over the motor cortex at 90% of resting motor threshold. Stimulation was delivered to the awake subjects 5 times a week for 3–4 weeks. Translocator protein (TSPO) expression was evaluated using Positron Emission Tomography and [11C]PBR28, and myo-inositol (mI) and N-acetyl-aspartate (NAA) concentrations were assessed with Magnetic Resonance Spectroscopy. Animals were then euthanized, and immunofluorescence staining was performed using antibodies against TSPO. Paired t-tests showed no significant changes in [11C]PBR28 measurements after stimulation. Similarly, no significant changes in mI and NAA concentrations were found. Post-mortem TSPO evaluation showed comparable mean immunofluorescence intensity after active TBS and sham delivery. The current study suggests that in healthy brains a clinical course of TBS, as evaluated with in-vivo imaging techniques (PET and MRS), did not measurably modulate the expression of glia related markers and metabolite associated with neural viability.
“…Glial cells, primarily astrocytes, regulate the quantities of extracellular glutamate ( Fan et al, 2023 ; Liu et al, 2023 ; Ferreira et al, 2024 ). Figure 3 illustrates and discusses the conceivable mechanism of MSG-induced neurotoxicity, respectively.…”
This systematic review analyzes monosodium glutamate (MSG) in the Alzheimer’s disease-like condition to enhance translational research. Our review seeks to understand how MSG affects the brain and causes degenerative disorders. Due to significant preclinical data linking glutamate toxicity to Alzheimer’s disease and the lack of a comprehensive review or meta-analysis, we initiated a study on MSG’s potential link. We searched PubMed, ScienceDirect, ProQuest, DOAJ, and Scopus for animal research and English language papers without time constraints. This study used the PRISMA-P framework and PICO technique to collect population, intervention or exposure, comparison, and result data. It was registered in PROSPERO as CRD42022371502. MSG affected mice’s exploratory behaviors and short-term working memory. The brain, hippocampus, and cerebellar tissue demonstrated neuronal injury-related histological and histomorphometric changes. A total of 70% of MSG-treated mice had poor nesting behavior. The treated mice also had more hyperphosphorylated tau protein in their cortical and hippocampus neurons. Glutamate and glutamine levels in the brain increased with MSG, and dose-dependent mixed horizontal locomotor, grooming, and anxiety responses reduced. MSG treatment significantly decreased phospho-CREB protein levels, supporting the idea that neurons were harmed, despite the increased CREB mRNA expression. High MSG doses drastically lower brain tissue and serum serotonin levels. In conclusion, MSG showed AD-like pathology, neuronal atrophy, and short-term memory impairment. Further research with a longer time span and deeper behavioral characterization is needed.Systematic review registration: https://www.crd.york.ac.uk/prospero/, identifier [CRD42022371502].
“…It is a technology that stimulates and identifies changes in the direction of the proton rotation axis that appear in the water that makes up the tissues of the organism [62,63]. Briefly, MRI uses magnets with a large magnetic field that drives the protons in the body to align with the field produced [64]. The protons are stimulated and fight against the strength of the magnetic field and when the radiofrequency field is turned off the protons align with the magnetic field and the sensors can identify the energy released.…”
Section: Insights From Neuroimaging On Exercise and Nutrition's Impactmentioning
This comprehensive review explores the dynamic relationship between sports, nutrition, and neurological health. Focusing on recent clinical advancements, it examines how physical activity and dietary practices influence the prevention, treatment, and rehabilitation of various neurological conditions. The review highlights the role of neuroimaging in understanding these interactions, discusses emerging technologies in neurotherapeutic interventions, and evaluates the efficacy of sports and nutritional strategies in enhancing neurological recovery. This synthesis of current knowledge aims to provide a deeper understanding of how lifestyle factors can be integrated into clinical practices to improve neurological outcomes.
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