Neuroscience
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Chronic pain is prevalent among aging adults. Epidemiologic evidence has demonstrated that individuals with chronic pain have accelerated memory decline and increased probability of dementia. ⋯ We validate this with multiple independent data sets and identify cortical microglia as a likely mechanism by which chronic pain can increase dementia risk. Our analyses support the molecular hypothesis for the role of chronic pain in cognitive decline and identifies several potential therapeutic targets.
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Theta oscillations in observers' temporal cortex index postural instability of point-light displays.
This study investigates whether postural equilibration follows the same principles of motor resonance as goal-oriented actions, namely, whether an individual activates the same neuronal substrates when experiencing postural perturbation as when observing another individual in this condition. To address this question, we examined electroencephalographic dynamics while subjects observed point-light displays featuring an unstable human display, a stable human display, and their respective scrambled counterparts lacking shape information and biological motion. We focused on theta band (4-7 Hz), which is a fundamental frequency for modulating brain activity during challenging balance tasks and reflects postural stability monitoring. ⋯ By contrast, the stronger theta response to the stable display as compared to the unstable one could be due to the difficulty of recognizing low-motion biological stimuli, or alternatively, to a facilitation of stimulus processing and strengthening of the mirroring response. The response facilitation for stable posture, coupled with a diminished response to the unstable display, could contribute to a broader mechanism mitigating postural threats and ensuring stable balance. Future investigations should leverage these findings to explore how posture-related responses correlate with perceptual and motor expertise, and to more clearly define these mechanisms during dynamic social interactions.
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Microinfarcts are widespread in the elderly, accompanied by varying degrees of cognitive decline. Continuous theta burst stimulation (cTBS) has been demonstrated to be neuroprotective on cognitive dysfunction, but the underlying cellular mechanism has been still not clear. In the present study, we evaluated the effects of cTBS on cognitive function and brain pathological changes in mice model of microinfarcts. ⋯ Our results showed that cTBS treatment significantly improved the spatial learning and memory, accelerated the efficiency of glymphatic clearance, up-regulated the AQP4 expression and improved the polarity distribution of AQP4 in microinfarcts mice. Besides, cTBS treatment increased the number of surviving neurons, whereas decreased the activated astrocytes and microglia. Our study suggested that cTBS accelerated glymphatic clearance and inhibited the excessive gliogenesis, which ultimately exerted neuroprotective effects on microinfarcts mice.
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The neuroinflammatory response promotes secondary brain injury after traumatic brain injury (TBI). Triggering receptor expressed on myeloid cells 1 (TREM1) is a key regulator of inflammation. However, the role of TREM1 in TBI is poorly studied. ⋯ Moreover, after TREM1 was inhibited, the secretion of the proinflammatory factors TNF-α and IL-1β was significantly reduced, while the secretion of the anti-inflammatory factors IL-4 and IL-10 was significantly increased. Additionally, inhibition of TREM1 by LP17 significantly reduced neuronal apoptosis and ameliorated nerve dysfunction in TBI model rats. In conclusion, our findings suggest that TREM1 enhances neuroinflammation and promotes neuronal apoptosis after TBI, and these effects may be partly mediated via the ERK/cPLA2 signalling pathway.
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Deficits in social communication and language development are a hallmark of autism spectrum disorder currently with no effective approaches to reduce the negative impact. Interventional studies using animal models have been very limited in demonstrating improved vocal communication. Autism has been proposed to involve metabolic dysregulation. ⋯ Composition of call categories and transitioning between individual call subtypes were more effectively altered to more closely align with the control group in juvenile BTBR mice. Together, our data provide further support to the hypothesis that metabolism-based dietary intervention could modify disease expression, including core symptoms, in autism. Future studies should tease apart the molecular mechanisms of KD's effects on vocalization.