Brain research
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Ten minutes of aerobic or resistance training can 'boost' executive function in older adults. Here, we examined whether the magnitude of the exercise benefit is influenced by exercise intensity. Older adults (N = 17: mean age = 73 years) completed a volitional test to exhaustion (VO2peak) via treadmill to determine participant-specific moderate (80% of lactate threshold (LT)), heavy (15% of the difference between LT and VO2peak) and very-heavy (50% of the difference between LT and VO2peak) exercise intensities. ⋯ Most notably, the post-exercise change in antisaccade RTs did not reliably vary with exercise intensity. Further, for each exercise intensity participants' cardiorespiratory fitness level was unrelated to the magnitude of the post-exercise executive benefit (ps > .13). Accordingly, an exercise duration as brief as 10-min provides a selective benefit to executive function in older adults across the continuum of moderate to very-heavy intensities.
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The present study aimed to investigate cerebral metabolic changes in a neuropathic pain model following deafferentation. A total of 24 Sprague-Dawley rats were included for modeling of right brachial plexus avulsion (BPA) through the posterior approach. As nerve injury would cause central sensitization and facilitate pain sensitivity in other parts of the body, thermal withdrawal latency (TWL) of the intact forepaw was assessed to investigate the level of pain perception following BPA-induced neuropathic pain. [Fluorine-18]-fluoro-2-deoxy-d-glucose (18F-FDG) positron emission tomography (PET) was applied to the brain before and after brachial plexus avulsion to explore metabolic changes in neuropathic pain following deafferentation. ⋯ Conversely, SUVs in multiple brain regions decreased, including the contralateral somatosensory cortex, ipsilateral cingulate cortex, and ipsilateral temporal association cortex. The Pearson correlation analysis showed that the SUVs of the contralateral anterodorsal hippocampus and ipsilateral dorsolateral thalamus were negatively related to the TWL of the intact forepaw, whereas the SUVs in the contralateral somatosensory cortex and ipsilateral cingulate cortex were positively related to it (p < 0.05). These findings indicate that upregulation of metabolism in the anterodorsal hippocampus and dorsolateral thalamus and downregulation metabolism in the contralateral somatosensory cortex and ipsilateral cingulate cortex could be a unique pattern of metabolic changes for neuropathic pain following brachial plexus avulsion.
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Randomized Controlled Trial
Effects of mild traumatic brain injury and post-traumatic stress disorder on resting-state default mode network connectivity.
Mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD) are common outcomes for service members. Abnormal connectivity within neural networks has been reported in the resting brain of mTBI and PTSD patients, respectively; however, the potential role of PTSD in changes to neural networks following injury has not been studied in detail. Using a data-driven approach, the present analysis aimed to elucidate resting state functional connectivity in the default mode network (DMN) in those with mTBI only and those with comorbid mTBI and PTSD. ⋯ For all subjects with mTBI, network connectivity correlated inversely with PTSD checklist score (p < 0.05). Additionally, distinct associations (p < 0.05) between medial prefrontal cortex connectivity and PTSD symptoms and, separately, posterior cingulate cortex connectivity and mTBI-related cognitive deficits were found. To our knowledge, this is the first study to report a differential relationship between DMN components and both post-traumatic symptoms and cognitive outcomes.
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Hypotension and low cerebral perfusion pressure are associated with low cerebral blood flow, cerebral ischemia, and poor outcomes after traumatic brain injury (TBI). Cerebral autoregulation is impaired after TBI, contributing to poor outcome. In prior studies, ERK mitogen activated protein kinase (MAPK) and ET-1 had been observed to be upregulated and contribute to impairment of cerebral autoregulation and histopathology after fluid percussion brain injury (FPI). ⋯ Results show that pial artery dilation in response to the Katp agonist cromakalim, the Kca agonist NS1619, PGE2 and the NO releaser sodium nitroprusside (SNP) were blocked by FPI, but such impairment was prevented by iNO administered at 2 h post injury. Protection lasted for at least 1 h after iNO administration was stopped. Using vasodilaton as an index of function, these data indicate that iNO prevents impairment of cerebral autoregulation and limits histopathology after TBI through protection of K channel function via blockade of ERK MAPK and ET-1.
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Alzheimer's disease (AD) is characterized by the classical hallmarks of Aβ-deposition and tau-pathology that are thought to ultimately lead to synapse and neuron loss. Although long known, neuroinflammation has recently attracted a substantial amount of attention by researchers due to genome wide association studies (GWAS) that identified microglia associated genes to be correlated with sporadic AD. Besides that, cholinergic degeneration and gamma-aminobutyric acid (GABA) abnormalities have been identified in the brains of AD patients already decades ago, but have not received much attention over the last ten years. ⋯ In this context, an imbalance between excitation and inhibition has been hypothesized to contribute to neuronal network dysfunction. Here, disturbances of cholinergic and GABAergic transmission might play a crucial role. In this review, we will focus on GABAergic dysfunction in AD and mouse models of AD and how those might relate to neuronal network aberration and memory impairment.