Neuroscience
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Sestrin2 (Sesn2) is a stress response protein which expresses neuroprotective characteristics in some neurodegenerative disorders. However, the impact of Sesn2 on the clinical outcome of stroke is unclear. The nuclear factor-erythroid 2 related factor 2/heme oxygenase-1 (Nrf2/HO-1) pathway is a key factor in angiogenesis, which aids in attenuating cerebral ischemia damage. ⋯ While Sesn2, Nrf2, HO-1, and VEGF were significantly increased following cerebral ischemia, overexpression of Sesn2 further increased their expression. After silencing Nrf2, the opposite effect was observed. These results imply that Sestrin2 may activate the Nrf2 / HO-1 pathway, leading to enhanced angiogenesis following photothrombotic cerebral ischemia.
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Temporal lobe epilepsy (TLE) is the commonest of adult epilepsies, often refractory to antiepileptic medications, whose prevention and treatment rely on understanding basic pathophysiological mechanisms in interlinked structures of the temporal lobe. The medial entorhinal area (MEA) is affected in TLE but mechanisms underlying hyperexcitability of MEA neurons require further elucidation. Previous studies have examined the role of the presubiculum (PrS) in mediating MEA pathophysiology but not the juxtaposed parasubiculum (Par). ⋯ These neurons experience significant reductions in synaptic inhibition and perish under chronic epileptic conditions. Connectivity between brain regions was deduced through changes in excitatory and inhibitory synaptic drive to neurons recorded in one region upon focal application of glutamate followed by NBQX to neurons in another using a microfluidic technique called CESOP and TLE-related circuit reorganization was assessed using data from normal and epileptic animals. The region-specific changes in Par and neighboring PrS and MEA together with their unexpected interactions are of significance in identifying ictogenic cells and circuits within the parahippocampal region and in unraveling pathophysiological mechanisms underlying TLE.
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Randomized Controlled Trial
The Role of S100B in Aerobic Training Efficacy in Older Adults with Mild Vascular Cognitive Impairment: Secondary Analysis of a Randomized Controlled Trial.
Aerobic training improves cognitive and brain outcomes across different populations and neurocognitive disorders of aging, including mild subcortical ischemic vascular cognitive impairment (SIVCI). However, little is known of the underlying mechanisms through which aerobic training exerts its beneficial effects on the brain. Recently, S100 calcium-binding protein B (S100B) has been proposed as a possible mediator of aerobic training. ⋯ At trial completion, aerobic training decreased circulating levels of S100B compared with usual care plus education. Furthermore, reduced S100B levels were associated with improved global cognitive function in those who received the aerobic exercise intervention. Together these findings suggest that S100B is a promising target mediating the beneficial effects of moderate-intensity aerobic training on brain health in older adults with mild SIVCI.
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Auditory verbal hallucinations (AVHs) frequently occur across multiple psychiatric diseases especially in schizophrenia (SCZ) patients. Functional imaging studies have revealed the hyperactivity of the auditory cortex and disrupted auditory-verbal network activity underlying AVH etiology. This review will firstly summarize major findings from both human AVH patients and animal models, with focuses on the auditory cortex and associated cortical/sub-cortical areas. ⋯ However, we can still extract useful information from animal SCZ models based on the disruption of auditory pathway during AVH episodes. Therefore, we will further interpolate the synaptic structures and molecular targets, whose dysregulation in SCZ models may be highly related with AVH episodes. As the last part, implications for future development of treatment strategies will be discussed.
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Neurobrucellosis, which is the most morbid form of brucellosis disease, presents with inflammatory signs and symptoms. Recent experimental evidence clearly indicates that deregulation of astrocytes and microglia caused by Brucella infection creates a microenvironment in the central nervous system (CNS) in which secretion of pro-inflammatory mediators lead to destabilization of the glial structure, the damage of the blood brain barrier (BBB) and neuronal demise. This review of Brucella interactions with cells of the CNS and the BBB is intended to present recent immunological findings that can explain, at least in part, the basis for the inflammatory pathogenesis of the nervous system that takes place upon Brucella infection.