Neuroscience
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Previous research has mapped out the brain regions that respond to semantic stimuli presented visually and auditorily, but there is debate about whether semantic representation is modality-specific (only written or only spoken) or modality-invariant (both written and spoken). The mechanism of semantic representation underlying native (L1) and second language (L2) comprehension in different modalities as well as how this mechanism is influenced by L2 proficiency, remains unclear. We used functional magnetic resonance imaging (fMRI) data from the OpenNEURO database to calculate neural pattern similarity across native and second languages (Spanish and English) for different input modalities (written and spoken) and learning sessions (before and after training). ⋯ Cross-language pattern similarity between L1 and L2 written words was observed in the right anterior temporal lobe. Brain-behavior correlations indicated that increased cross-language pattern similarity between L1 and L2 written words in the right anterior temporal lobe was associated with L2 written word comprehension. This study identified an effective neurofunctional predictor related to L2 written word comprehension.
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Our recent study revealed that fluorescent lamp light can penetrate deep into the brain of mice and rats leading to the development of typical histological characteristics associated with Parkinson's disease such as the loss of dopamine neurons in the substantia nigra. Monochromatic LED lights were thus used in this work to deepen our knowledge on the effects of the major wavelength peaks of fluorescent light on mouse and human dopaminergic cells. In particular, we exposed immortalized dopaminergic MN9D neuronal cells, primary cultures of mouse mesencephalic dopaminergic cells and human dopaminergic neurons differentiated from induced pluripotent stem cells (hiPSC) to different LED light wavelengths. ⋯ Notably, differentiated MN9D dopaminergic cells, which closely resemble mature dopamine neuronal phenotype, acutely exposed for 3 h at 610 nm, showed a clear increase in ROS production and cytotoxicity compared to controls undifferentiated MN9D cells. These increases were even more pronounced by the co-treatment with the oxidative agent H2O2. Collectively, these findings suggest that specific wavelengths, particularly those capable of penetrating deep into the brain, could potentially pose an environmental hazard in relation to Parkinson's disease.
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Alcohol hangover is the combination of negative mental and physical symptoms which can be experienced after a single episode of alcohol consumption, starting when blood alcohol concentration approaches zero. We previously demonstrated that hangover provokes mitochondrial dysfunction, oxidative stress, imbalance in antioxidant defenses, and impairment in cellular bioenergetics. Chronic and acute ethanol intake induces neuroapoptosis but there are no studies which evaluated apoptosis at alcohol hangover. ⋯ Caspase 3, 8 and 9 protein expressions were 32%, 33% and 20% respectively enhanced and the activity of caspase 3 and 6 was 30% and 20% increased also due to the hangover condition. Moreover, 38% and 32% increments were found in PARP1 and p53 protein expression respectively and on the contrary, SIRT-1 was almost 50% lower than controls due to the hangover condition. The present work demonstrates that alcohol after-effects could result in the activation of mitochondrial and non-mitochondrial apoptosis pathways.
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The M1 polarization of microglia, followed by the production of pro-inflammatory mediators, hinders functional recovery after spinal cord injury (SCI). Our previous study has illuminated that specificity protein 1 (Sp1) expression is increased following SCI, whereas the function and regulatory mechanism of Sp1 during M1 polarization of microglia following SCI remain unknown. RNA binding protein, HuR, has been shown to be up-regulated in the injured spinal cord through analysis of the GEO database. ⋯ Enhanced expression of HuR was observed in both SCI mice and LPS-treated BV2 cells, while Sp1 knockdown restrained M1 polarization of microglia and its associated inflammation by inhibiting the NF-κB signaling pathway. Silencing Sp1 also suppressed microglia activation and its mediated inflammatory response, which could be reversed by overexpression of HuR. In conclusion, silencing Sp1 restrains M1 polarization of microglia through the HuR/NF-κB axis, leading to neuroprotection, and thus promotes functional restoration following SCI.
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Recent researches have noted many changes of short-term dynamic modalities in mild cognitive impairment (MCI) patients' brain functional networks. In this study, the dynamic functional brain networks of 82 MCI patients and 85 individuals in the normal control (NC) group were constructed using the sliding window method and Pearson correlation. The window size was determined using single-scale time-dependent (SSTD) method. ⋯ R. This study on DFC states explores changes in the brain functional networks of patients with MCI from the perspective of alterations in the community structures of DFC states. The findings could provide new insights into the pathological changes in the brains of MCI patients.