Neuroscience
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Spinal cord injury (SCI) is a central nervous system trauma that can cause severe neurological impairment. A series of pathological and physiological changes after SCI (e.g., inflammation, oxidative stress, apoptosis, and mitochondrial dysfunction) promotes further deterioration of the microenvironment at the site of injury, leading to aggravation of neurological function. ⋯ A comprehensive understanding of the function and regulatory mechanism of Nrf2 in the pathophysiology of SCI will aid in the development of targeted therapeutic strategies for SCI. This review discusses the roles of Nrf2 in SCI, with the aim of aiding in further elucidation of SCI pathophysiology and in efforts to provide Nrf2-targeted strategies for the treatment of SCI.
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The beneficial effects of exercise on human brain function have been demonstrated in previous studies. Myokines secreted by muscle have attracted increasing attention because of their bridging role between exercise and brain health. Regulated by PPARγ coactivator 1α, fibronectin type III domain-containing protein 5 releases irisin after proteolytic cleavage. ⋯ Meanwhile, irisin has anxiolytic and antidepressant effects. The potential therapeutic effects of irisin in epilepsy and pain have been initially revealed. Due to the pleiotropic and beneficial properties of irisin, the possibility of irisin treating other neurological diseases could be gradually explored in the future.
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Endemic arsenism is a worldwide health problem. Chronic arsenic exposure results in cognitive dysfunction due to arsenic and its metabolites accumulating in hippocampus. ⋯ However, excessive NMDARs activity contributes to exitotoxicity and synaptic plasticity impairment. Here, we provide an overview of the mechanisms that NMDARs and their downstream signaling pathways mediate synaptic plasticity impairment due to arsenic exposure in hippocampal neurons, ways of arsenic exerting on NMDARs, as well as the potential therapeutic targets except for water improvement.
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Catecholaminergic transmission plays an essential role in both physiological and pathological cognitive functions. Plastic changes subserving learning and memory processes are highly dependent on catecholaminergic activity, altering their function and impacting cognition. This review assesses changes in the dopaminergic and norepinephrine systems as part of the mechanisms underlying cognitive impairment in Alzheimer's disease as associated with metabolic dysfunctions such as type 2 diabetes, metabolic syndrome, and neuroinflammation and peripheral inflammation. Understanding the role of catecholaminergic systems in these conditions is relevant for identifying etiological factors that could advance diagnostic and therapeutic approaches for ameliorating cognitive alterations, disease onset, and progression.
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Episodic meal-related memories provide the brain with a powerful mechanism for tracking and controlling eating behavior because they contain a detailed record of recent energy intake that likely outlasts the physiological signals generated by feeding bouts. This review briefly summarizes evidence from human participants showing that episodic meal-related memory limits later eating behavior and then describes our research aimed at investigating whether hippocampal neurons mediate the inhibitory effects of meal-related memory on subsequent feeding. ⋯ I describe our evidence showing that ingestion activates the molecular processes necessary for synaptic plasticity and memory during the early postprandial period, when the memory of the meal would be undergoing consolidation, and then summarize our findings showing that neural activity in dHC neurons is critical during the early postprandial period for limiting future intake. Collectively, our evidence supports the hypothesis that dHC neurons mediate the inhibitory effects of ingestion-related memory on future intake and demonstrates that post-experience memory modulation is not confined to artificial laboratory memory tasks.