Neuroscience
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A spontaneous mutation of the disrupted in schizophrenia 1 (Disc1) gene is carried by the 129S inbred mouse strain. Truncated DISC1 protein in 129S mouse synapses impairs the scaffolding of excitatory postsynaptic receptors and leads to progressive spine dysgenesis. In contrast, C57BL/6 inbred mice carry the wild-type Disc1 gene and exhibit more typical cognitive performance in spatial exploration and executive behavioral tests. ⋯ Analysis of pyr/int connectivity revealed a significant delay in synaptic transmission for 129S putative pairs. Sampled 129S pyr/int pairs also had lower detectability index scores than B6 putative pairs. Therefore, the spontaneous Disc1 mutation in the 129S strain attenuates the firing of putative pyr CA1 neurons and impairs spike timing fidelity during cognitive tasks.
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Recent studies show that overlapping community structure is an important feature of the brain functional network. However, alterations in such overlapping community structure in Alzheimer's disease (AD) patients have not been examined yet. In this study, we investigate the overlapping community structure in AD by using resting-state functional magnetic resonance imaging (rs-fMRI) data. ⋯ In particular, the frontal-parietal and basal ganglia networks exhibit significant differences between the two groups. A machine learning framework proposed in this paper for AD detection achieved an accuracy of 76.7% when using the detected community strengths of the frontal-parietal and basal ganglia networks only as input features. These findings provide novel insights into the understanding of pathological changes in the brain functional network organization of AD and show the potential of the community structure-related features for AD detection.
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Cerebral ischemia/reperfusion (I/R) injury is the continuation and deterioration of ischemic injury, and there are no effective treatment strategies for this condition. It has been reported that microRNAs (miRNAs) are considered as potential targets to protect the brain against I/R injury. Previous studies have shown that miR-489-3p plays a vital role in regulating apoptosis of neurons. miR-489-3p is considered as a potential target to protect the brain against I/R injury-induced neuron apoptosis. ⋯ Silencing of HDAC2 showed a neuroprotective effect against OGD/R injury in vitro. Overexpression of HDAC2 significantly attenuated the protective effects of miR-489-3p mimics on cell injury in vitro. Our results revealed that the upregulation of miR-489-3p attenuated cerebral I/R injury by negatively regulating HDAC2.