Neuroscience
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Chronic insomnia (CI) is a common sleep disorder in middle-aged and elderly individuals. Long-term sleep deprivation can lead to physical, mental, and cognitive damage. Resting-state networks (RSNs) in the brain are closely linked to cognition and behavior. ⋯ Moreover, FC values in the right middle frontal gyrus within right frontal parietal network of CI-I patients were negatively correlated with the Mini-Mental State Examination scores. These results may explain hyperarousal, attention deficit and motor impairments in CI patients. Furthermore, the aberrant alterations of RSNs in CI-I patients may play a crucial role in the onset and progression of cognitive impairment in CI patients.
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Patients experiencing severe hemiplegia following a stroke struggle to rehabilitate their affected limbs. Cross-education (CE) training emerges as a promising rehabilitation method due to its safety, simplicity, low risk, and ability to effectively improve muscle strength in the affected limb. However, controversy surrounds the neural mechanisms and clinical applications of CE. ⋯ SIGNIFICANCE STATEMENT: Exploring the neural mechanisms underlying one session of 50% MVC strength training with less-affected hand sheds light on a safe therapy. The study enhances our understanding of less-affected hand training and investigates the feasibility as a future rehabilitation approach. Analyzing how one session of 50% MVC strength training with less-affected hand affects brain activation and connectivity could lead to more tailored and effective rehabilitation strategies.
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Ginsenoside Rg1 (Rg1) has been shown to treat a variety of human diseases, including Alzheimer's disease (AD). However, its mechanism in AD needs further investigation. Microglial cells (BV2) were treated with Aβ1-42 to induce AD cell models. ⋯ GATA4 interacted with PDE4A, and GATA4 facilitated Aβ1-42-induced BV2 cell injury by increasing PDE4A expression. Besides, GATA4 knockdown reduced PDE4A protein expression and inactivated PI3K/AKT axis, while these effects were abolished by PDE4A overexpression. In conclusion, our data suggested that Ginsenoside Rg1 inhibited microglial cell apoptosis and inflammation to attenuate AD progression by regulating the GATA4/PDE4A/PI3K/AKT axis.
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Controversy persists regarding the representation of linguistically negated actions, specifically concerning activation and inhibitory mechanisms in the motor system, and whether negated action sentences evoke an initial motor simulation of the action to be negated. We conducted two experiments probing corticospinal excitability (CSE) and short-interval intracortical inhibition (SICI) in the primary motor cortex at different latencies while reading affirmative and negative action sentences. In experiment one, twenty-six participants read action and non-action sentences in affirmative or negative forms. ⋯ Negated action sentences showed the same motor excitability as affirmed action sentences with no additional inhibition at early latencies. These results lend support for the idea that actions to be negated are initially simulated within the motor system. Neural differences between affirmative and negative action sentences may occur outside the primary motor cortex.
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Reductions in circulating estrogens can contribute to cognitive decline, in part by impairing mitochondrial function within the hippocampal region. The entorhinal cortex provides the hippocampus with its main cortical inputs. To assess the impact of estrogen deficiency on mitochondrial respiration and synaptic proteins in the entorhinal cortex, female wildtype rats received either sham surgery, bilateral ovariectomy, or ovariectomy with implantation of a subdermal capsule to maintain low levels of circulating 17β-estradiol (E2). ⋯ Further, the ovariectomy-induced changes in mitochondrial proteins were associated with reductions in postsynaptic density protein 95 (PSD95) and the presynaptic protein synaptophysin. There were no changes in mitochondrial or synaptic proteins in ovariectomized animals that received E2 supplementation. Our findings indicate that reductions in circulating 17β-estradiol induced by ovariectomy disrupt mitochondrial functions in the entorhinal cortex, and suggest that a resulting increase in oxidative stress contributes to the degradation in synaptic proteins that may affect cognitive functions mediated by the hippocampal region.