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[This corrects the article DOI 10.3389/fnins.2020.00874.].Methamphetamine (MA), an illicit drug abused worldwide, leads to cognitive impairment and memory loss. However, the detailed mechanisms of MA-induced neurologic impairment are still unclear. The present study aimed to investigate the mechanisms of MA-induced inhibition of memory acquisition from the perspective of endoplasmic reticulum (ER) stress. ER stress, caused by the accumulation of wrongly folded proteins in the ER, is important for new protein synthesis, which further influence the formation of long-term memory. A subacute MA poisoning model of mice was established and several behavioral experiments were performed, including elevated plus maze, Morris water maze, electro-stimulus Y-maze, and novel object recognition tasks. The present results suggested that 4 days exposure to MA induced significant memory loss. Whereas, this damage to memory formation could be protected when mice were pre-treated with ER stress inhibitor, tauroursodeoxycholic acid (TUDCA). The results of Western blotting showed that subacute exposure to MA increased the expression levels of ER stress marker proteins, such as binding immunoglobulin protein, phosphorylated eukaryotic translation initiation factor 2α, cyclic AMP-dependent transcription factor (ATF)-4, ATF-6, and CCAAT-enhancer binding protein homologous protein. Meanwhile, the enhanced expression levels of these proteins were reversed by TUDCA, indicating that MA administration induced memory loss by evoking ER stress in the hippocampus. We also found that MA inhibited the induction of long-term potentiation (LTP) in the hippocampus. Nevertheless, LTP could be induced when mice were pre-treated with TUDCA. In conclusion, MA inhibited long-term memory acquisition and synaptic plasticity via ER stress.Sleep is crucial for optimal well-being, and sex differences in sleep quality have significant implications for women's health. We review the current literature on sex differences in sleep, such as differences in objective and subjective sleep measures and their relationship with aging. We then discuss the convincing evidence for the role of ovarian hormones in regulating female sleep, and survey how these hormones act on a multitude of brain regions and neurochemicals to impact sleep. Lastly, we identify several important areas in need of future research to narrow the knowledge gap and improve the health of women and other understudied populations.Alzheimer's disease (AD) is the most common cause of dementia, affecting millions of people worldwide, and no cure is currently available. The major pathological hallmarks of AD are considered to be amyloid beta plaques and neurofibrillary tangles, generated by respectively APP processing and Tau phosphorylation. Recent evidence imply that glycosylation of these proteins, and a number of other AD-related molecules is altered in AD, suggesting a potential implication of this process in disease pathology. In this review we summarize the understanding of glycans in AD pathogenesis, and discuss how glycobiology can contribute to early diagnosis and treatment of AD, serving as potential biomarkers and therapeutic targets. Furthermore, we look into the potential link between the emerging topic neuroinflammation and glycosylation, combining two interesting, and until recent years, understudied topics in the scope of AD. Lastly, we discuss how new model platforms such as induced pluripotent stem cells can be exploited and contribute to a better understanding of a rather unexplored area in AD.The neuronal cascade related to the perception of either purely olfactory or trigeminal airborne chemicals has been investigated using electroencephalography (EEG) microstate analyses and source localization. However, most airborne chemicals are bimodal in nature, encompassing both properties. Moreover, there is an ongoing debate regarding whether there is one dominant nostril, and this could be investigated using these multichannel EEG methods. In this study, 18 right-handed, healthy participants (13 females) were monorhinally stimulated using an olfactometer with the bimodal component acetic acid during continuous EEG recording. Participants indicated the side of stimulation, the confidence in their decision, and rated the strength of the evoked perception. EEG microstate clustering determined four distinct maps and successive backfitting procedures, and source estimations revealed a network that evolved from visual-spatial processing areas to brain areas related to basic olfactory and trigeminal sensations (e.g., thalamus, cingulate cortex, insula, parahippocampal, and pre-/post-central gyri) and resulted in activation of areas involved in multisensory integration (e.g., frontal-temporal areas). Right-nostril stimulation was associated with faster microstate transition and longer involvement of the superior temporal gyrus, which was previously linked to chemical localization and provides evidence for a potential nostril dominance. The results describe for the first time the processing cascade of bimodal odor perception using microstate analyses and demonstrate its feasibility to further investigate potential nostril dominance.Over the past decades, the human life span has dramatically increased, and therefore, a steady increase in diseases associated with age (such as Alzheimer's disease and Parkinson's disease) is expected. 5'-N-Ethylcarboxamidoadenosine mouse In these neurodegenerative diseases, there is a cognitive decline and memory loss, which accompany increased systemic inflammation, the inflamm-aging, and the insulin resistance. Despite numerous studies of age-related pathologies, data on the contribution of brain insulin resistance and innate immunity components to aging are insufficient. Recently, much research has been focused on the consequences of nutrients and adiposity- and nutrient-related signals in brain aging and cognitive decline. Moreover, given the role of metainflammation in neurodegeneration, lifestyle interventions such as calorie restriction may be an effective way to break the vicious cycle of metainflammation and have a role in social behavior. The various effects of calorie restriction on metainflammation, insulin resistance, and neurodegeneration have been described.
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