Neuroscience
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Past research has demonstrated that field dependence-independence (FDI) can affect academic performance, selective attention, and working memory. However, the underlying mechanism of how FDI modulates selective attention and working memory is still unclear. ⋯ These results indicated that FI participants can filter out task-irrelevant information more efficiently than FD participants. The main difference between FD and FI individuals is their inhibition function.
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Mindfulness is typically defined as nonjudgmental awareness of experiences in the present moment, which is beneficial for mental and physical well-being. Previous studies have identified multiple regions in the default mode network (DMN) that are involved in mindfulness, but little is known about how these regions work collaboratively as a network. ⋯ Post-hoc analyses of these two nodes further revealed that graph-based nodal properties of the thalamus, not the PCC, were negatively correlated with trait mindfulness, suggesting that a low involvement of the thalamus in the DMN is relevant for high trait mindfulness. Our findings not only suggest the thalamus as a switch between mind-wandering and mindfulness, but also invite future studies on mechanisms of how mindfulness produces beneficial effects by modulating the thalamus.
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Intraneuronal accumulation of beta-amyloid protein (Aβ) is an early pathological change in Alzheimer's disease (AD). Recent studies demonstrate that α7 nicotinic acetylcholine receptor (α7nAChR) binds to soluble Aβ with a high affinity. In vitro and in vivo experiments also show that Aβ activates p38 MAPK and ERK1/2 signaling pathways via the α7nAChR. ⋯ Our data demonstrate that Aβ1-42 induces an α7nAChR-dependent pathway that relates to the activation of p38 MAPK and ERK1/2, resulting in internalization of Aβ1-42. Our findings suggest that α7nAChR and MAPK signaling pathways play an important role in the uptake and accumulation of Aβ1-42 in SH-SY5Y cells. Blockade of α7nAChR may have a beneficial effect by limiting intracellular accumulation of amyloid in AD brain and serves a potential therapeutic target for AD.
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Accumulation of hypoxia-inducible transcription factors (HIFs) by prolyl-4-hydroxylase inhibitors (PHI) has been suggested to induce neuroprotection in the ischemic rodent brain. We aimed to investigate in vivo effects of a novel PHI on HIF-regulated neurotrophic and pro-apoptotic factors in the developing normoxic and hypoxic mouse brain. ⋯ PHI treatment modulates neurotrophic factors known to be crucially involved in hypoxia-induced cerebral adaptive mechanisms as well as early brain maturation. Pre-treatment with FG-4497 seems to protect the developing brain from hypoxia-induced apoptosis. Present observations provide basic information for further evaluation of neuroprotective properties of PHI treatment in hypoxic injury of the developing brain. However, potential effects on maturational processes need special attention in experimental research targeting HIF-dependent neuroprotective interventions during the very early stage of brain development.
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Alzheimer's disease (AD) is the most common and devastating neurodegenerative disease. The etiology of AD has yet to be fully understood, and common treatments remain largely non-efficacious. The amyloid hypothesis posits that extracellular amyloid-β (Aβ) deposits are the fundamental etiological factor of the disease. ⋯ Chronic exposure to (PhSe)2 attenuated oxidative stress induced by Aβ1-42, with concomitant recovery of associative learning memory in C. elegans. Additionally, (PhSe)2 decreased Aβ1-42 transgene expression, suppressed Aβ1-42 peptide, and downregulated hsp-16.2 by reducing the need for this chaperone under Aβ1-42-induced toxicity. These observations suggest that (PhSe)2 plays an important role in protecting against oxidative stress-induced toxicity, thus representing a promising pharmaceutical modality that attenuates Aβ1-42 expression.