Neuroscience
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Alzheimer's disease (AD) is a chronic neurological disorder with high morbidity. Exercise is one of the effective ways to ameliorate AD. In this study, we assessed the effects of exercise on cognition and inflammation and studied the role of miR-148a-3p in AD. ⋯ MiR-148a-3p silencing reversed these abovementioned tendencies. Patients with AD exhibited a low level of miR-148a-3p, which was increased after exercise. Therefore, exercise might improve the cognitive function and memory of mice with AD by upregulating miR-148a-3p.
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Locomotor movements in mammals are generated by neural networks, situated in the spinal cord, known as central pattern generators (CPGs). Recently, significant strides have been made in the genetic identification of interneuronal components of the locomotor CPG and their specific function. Despite this progress, a population of interneurons that is required for locomotor rhythmogenesis has yet to be identified, and it has been suggested that subsets of interneurons belonging to several genetically-defined populations may be involved. ⋯ Focal application of 5-hydroxytryptamine creatine sulfate complex (5-HT) and N-methyl-D-aspartate (NMDA) to the central canal of the rostral lumbar segments of newborn male and female mouse spinal cords quickly generates a robust pattern of fictive locomotion, while inhibition or ablation of neurons in this region disrupts the locomotor rhythm in both rostral and caudal lumbar segments. When applied to the central canal at caudal lumbar levels a higher volume of 5-HT and NMDA are required to elicit fictive locomotion, while inhibition of neurons surrounding the central canal at caudal levels again interrupts rhythmic activity at local segmental levels with minimal effects rostrally. The results of this study indicate that interneurons in the most medial laminae of the neonatal mouse spinal cord are both necessary and sufficient for the generation of locomotor activity, and suggests that this is the region where the rhythm generating core of the locomotor CPG resides.
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of the 2019 coronavirus disease (COVID-19), has affected more than 20 million people in Brazil and caused a global health emergency. This virus has the potential to affect various parts of the body and compromise metabolic functions. The virus-mediated neural inflammation of the nervous system is due to a storm of cytokines and oxidative stress, which are the clinical features of Alzheimer's disease (AD). ⋯ The cholinergic system, through neurons and the neurotransmitter acetylcholine (ACh), modulates various physiological pathways, such as the response to stress, sleep and wakefulness, sensory information, and the cognitive system. Patients with AD have low concentrations of ACh; hence, therapeutic methods are aimed at adjusting the ACh titers available to the body for maintaining functionality. Herein, we focused on acetylcholinesterase inhibitors, responsible for the degradation of ACh in the synaptic cleft, and muscarinic and nicotinic receptor agonists of the cholinergic system owing to the therapeutic potential of the cholinergic anti-inflammatory pathway in AD associated with SARS-CoV-2 infection.
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Diabetes is frequently accompanied by cognitive impairment with insidious onset, and progressive cognitive and behavioral changes. β-1, 3-galactosyltransferase 2 (B3galt2) contributes to glycosylation, showing a clue for neuronal apoptosis, proliferation and differentiation. However, the role of B3galt2 in diabetic cognitive dysfunction (DCD) has not been investigated. In the present study, we aimed to explore the role of B3galt2 in DCD. ⋯ Importantly, the expression of F3/Contactin can be regulated by the manipulation of B3galt2, overexpression of which assuaged hippocampal neuronal damage, protected the synapsin, and reduced neuronal apoptosis in diabetic mice. Interestingly, SAL alleviated DCD and reversed the expression of B3galt2 in diabetic C57BL/6J mice. These findings indicate that inhibition of B3galt2/F3/Contactin pathway contributes to DCD, and participates in SAL reversed DCD.
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In the present study, we examined adverse effects of metals and metalloids in the Cerebral cortex (CC) and Cerebellum (CE). Group 1 comprised from the controls while other four groups of male Wistar rats were treated with following pattern: Group II (Heavy Metal Mixture HMM only: PbCl2, 20 mg·kg-1; CdCl2, 1.61 mg·kg-1; HgCl2, 0.40 mg·kg-1, and NaAsO3,10 mg·kg-1), Groups III (HMM + ZnCl2); Group IV (HMM + Na2SeO3) and Group V (HMM + ZnCl2 + Na2SeO3) for 60 days per os. HMM promoted oxidative stress in the CC and CE of treated rats compared to controls; moreover, exposure to HMM led to increased activity of the AChE and pro-inflammatory cytokines; also, HMM promoted accumulation of caspase 3 and other transcriptional factors such as Nrf2 and decreased levels of Hmox-1. ⋯ HMM exposed rats had considerably less escape dormancy than controls. Histopathological analysis revealed moderate cell loss at the intermediate (Purkinje cell) and granular layer. Zinc and selenium supplementations could reverse adverse effects of heavy metals at various cellular levels in neurons.