Neuroscience
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Parthanatos is a modality of regulated cell death initiated by poly(ADP-ribose) polymerase 1 (PARP-1) hyperactivation and characterized by apoptosis inducing factor (AIF)-dependent and microphage migration inhibitory factor (MIF)-dependent DNA degradation. It is a caspase-independent, mitochondrial-linked paradigm of cell death and has been demonstrated to be related to the pathogenesis of various nervous system diseases. An in-depth understanding of the role that parthanatos plays in the pathological processes of these diseases can provide new targets for nervous system diseases treatments. In this review, on the basis of parthanatos mechanism, the involvement of parthanatos in the pathogenesis of nervous system diseases including neurodegenerative disorders, cerebrovascular diseases, spinal cord injury and glioma will be summarized in detail.
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Dendrite-targeting somatostatin-expressing interneurons (SST-INs) powerfully control signal integration and synaptic plasticity in pyramidal dendrites during cortical development. We previously showed that synaptic transmission from SST-INs to pyramidal cells (PCs) (SST-IN → PC) in the mouse visual cortex suddenly declined at around the second postnatal week. However, it is unclear what specific postsynaptic mechanisms underlie this developmental change. ⋯ Apart from pharmacological test, we observed that SST-IN → PC synapses did indeed contain α5-GABAARs by immunogold labeling for electron microscopy. More importantly, coinciding with the weakening of SST-IN → PC synaptic transmission, the number of α5-GABAAR particles in SST-IN → PC synapses significantly decreased at around the second postnatal week. Together, these data indicate that α5-GABAARs are involved in synaptic transmission from SST-INs to PCs in the neocortex, and are significantly diminished around the second postnatal week.
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The behavioral, cognitive, and sensory difficulties experienced by individuals exposed to alcohol prenatally currently fail to provide early identification for fetal alcohol spectrum disorder (FASD). Attempting to advance this pursuit through a multivariate analysis, we collected magnetoencephalography (MEG) data during auditory, somatosensory, visual paradigms, DTI, and behavior in adolescents ages 12-21 years (FASD: N = 13; HC: N = 20). We assessed the relationship between brain function (MEG) and structure (fractional anisotropy (FA)) utilizing joint independent component analysis (jICA), and examined how this measure relates to behavior. ⋯ Interestingly, this relationship is lacking in FASD (r = 0.009, p = 0.979). Also, component 5 loading factor negatively correlated with impulsivity (r = -0.527, p = 0.002), indicating that stronger function-structure associations were associated with individuals with lower impulsivity. These findings suggest that multimodal integration of MEG and FA provides novel associations between structure and function that may help differentiate adolescents with FASD from HC.
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Randomized Controlled Trial
Failure to Improve Verbal Fluency with Transcranial Direct Current Stimulation.
Previous studies in healthy populations have provided equivocal evidence whether the application of anodal transcranial direct current stimulation (tDCS) over the left prefrontal cortex (PFC) can improve performance in verbal fluency tasks. In this double-blind, randomised within-participant study, we investigated whether anodal tDCS over the left PFC improves verbal fluency performance relative to sham tDCS. Forty eight healthy native German speakers performed two verbal fluency tasks after having received 20 min of anodal or sham tDCS over the left PFC. ⋯ Overall, the current study found no evidence that verbal fluency performance in healthy speakers could be improved by excitatory stimulation of the left PFC. We argue that previously observed positive effects could be false positives and should be interpreted with caution. The findings from the current study thus cast further doubt on the utility of tDCS in enhancing cognitive performance in the healthy (young) brain.
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Cerebral small vessel disease (CSVD) is a common disease among elderly individuals and recognized as a major cause of vascular cognitive impairment. Recent studies demonstrated that CSVD is a disconnection syndrome. However, due to the covert neurological symptoms and subtle changes in clinical performance, the connection alterations during the stage of preclinical cognitive impairment (PCI) and mild cognitive impairment (MCI) are usually neglected and still largely unknown. ⋯ Moreover, in all CSVD patients, the strength of the rich-club, feeder and local connections was significantly correlated with multiple cognitive scores, especially in attention, executive, and memory domains; while in MCI patients, only the strength of the rich-club connections was significantly correlated with cognition. Furthermore, based on the network-based statistic analysis, we also identified distinct network component disruption pattern between the PCI group and the MCI group, validating the results described above. These results suggest a disruption pattern from peripheral to central connections with the change of cognitive status, shedding light on the early identification and the underlying disruption of CSVD.