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Part regarding Glycation throughout Type 2 Diabetes Mellitus and its particular Elimination via Nymphaea Species.
The plasma SOD were negatively correlated with H&Y, total UPDRS, UPDRS (I), UPDRS (II), and UPDRS (III) scores, but positively correlated with MoCA and MMSE scores. Besides, hsCRP was negatively correlated with MoCA; while total cholesterol, HDL-C and LDL-C were positively correlated with the MoCA, respectively. Conclusion Our findings suggest that lower SOD along with cholesterol, HDL-C and LDL-C, and higher hsCRP levels might be important markers to assess the PD severity. A better understanding of SOD and hsCRP may yield insights into the pathogenesis of PD. Copyright © 2020 Yang, Chang, Que, Weng, Deng, Wang, Huang, Xie, Wei, Yang, Li, Ma, Zhou, Tang, Mok, Zhu and Wang.Human brain evolution toward complexity has been achieved with increasing energy supply as the main adaptation in brain metabolism. Energy metabolism, like other biochemical reactions in aerobic cells, is under enzymatic control and strictly regulated. Nevertheless, physiologically uncontrolled and deleterious reactions take place. It has been proposed that these reactions constitute the basic molecular mechanisms that underlie the maintenance or loss-of-function of neurons and, by extension, cerebral functions during brain aging. In this review article, we focus attention on the role of the nonenzymatic and irreversible adduction of fumarate to the protein thiols, which leads to the formation of S-(2-succino)cysteine (2SC; protein succination) in the human brain. In particular, we first offer a brief approach to the succination reaction, features related to the specificity of protein succination, methods for their detection and quantification, the bases for considering 2SC as a biomarker of mitochondrial stress, the succinated proteome, the cross-regional differences in 2SC content, and changes during brain aging, as well as the potential regulatory significance of fumarate and 2SC. We propose that 2SC defines cross-regional differences of metabolic mitochondrial stress in the human brain and that mitochondrial stress is sustained throughout the healthy adult lifespan in order to preserve neuronal function and survival. Copyright © 2020 Jové, Pradas, Mota-Martorell, Cabré, Ayala, Ferrer and Pamplona.The association between physical fitness and cognitive performance has been widely investigated in the literature. However, the neurophysiological mechanisms underlying this relationship are not yet clear. Here, we aim to evaluate the interactions between executive function measures, heart rate variability (HRV), and physical fitness in the context of the neurovisceral integration (NVI) theory. Twenty-eight healthy elderly subjects (>60 years) were submitted to evaluation of executive performance with three computerized tests the N-back test measured working memory capacity, the Stroop Color test evaluated inhibitory control and selective attention, and the Wisconsin Card Sorting Test (WCST) evaluated abstract reasoning and cognitive flexibility. check details We also used the Physical Testing Battery for the Elderly to measure aerobic capacity, dynamic balance, upper body flexibility, and handgrip strength. Our results confirm the relationship between executive function and physical fitness, particularly between working memory, cardiorespiratory fitness, and dynamic balance. We also demonstrate an association between executive performance and HRV in older people, corroborating previous results from other groups obtained in young adults. However, our regression models did not indicate that HRV mediates the relationship between cognition and physical fitness in the elderly, suggesting that age-related degeneration of autonomic control can affect aspects of NVI in this population. Copyright © 2020 Matos, Vido, Garcia, Lopes and Pereira.Normative aging is known to affect how decisions are made in risky situations. Although important individual variability exists, on average, aging is accompanied by greater risk aversion. Here the behavioral and neural mechanisms of greater risk aversion were examined in young and old rats trained on an instrumental probability discounting task. Consistent with the literature, old rats showed greater discounting of reward value when the probability of obtaining rewards dropped below 100%. Behaviorally, reward magnitude discrimination was the same between young and old rats, and yet these same rats exhibited reduced sensitivity to positive, but not negative, choice outcomes. The latter behavioral result was congruent with additional findings that the aged ventral tegmental neurons (including dopamine cells) were less responsive to rewards when compared to the same cell types recorded from young animals. In sum, it appears that reduced responses of dopamine neurons to rewards contribute to aging-related changes in risky decisions. Copyright © 2020 Tryon, Baker, Long, Rapp and Mizumori.Dihydroartemisinin (DHA) is an active metabolite of sesquiterpene trioxane lactone extracted from Artemisia annua, which is used to treat malaria worldwide. DHA can activate autophagy, which is the main mechanism to remove the damaged cell components and recover the harmful or useless substances from eukaryotic cells and maintain cell viability through the autophagy lysosomal degradation system. Autophagy activation and autophagy flux correction are playing an important neuroprotective role in the central nervous system, as they accelerate the removal of toxic protein aggregates intracellularly and extracellularly to prevent neurodegenerative processes, such as Alzheimer's disease (AD). In this study, we explored whether this mechanism can mediate the neuroprotective effect of DHA on the AD model in vitro and in vivo. Three months of DHA treatment improved the memory and cognitive impairment, reduced the deposition of amyloid β plaque, reduced the levels of Aβ40 and Aβ42, and ameliorated excessive neuron apoptosis in APP/PS1 mice brain. In addition, DHA treatment increased the level of LC3 II/I and decreased the expression of p62. After Bafilomycin A1 and Chloroquine (CQ) blocked the fusion of autophagy and lysosome, as well as the degradation of autolysosomes (ALs), DHA treatment increased the level of LC3 II/I and decreased the expression of p62. These results suggest that DHA treatment can correct autophagic flux, improve autophagy dysfunction, inhibit abnormal death of neurons, promote the clearance of amyloid-β peptide (Aβ) fibrils, and have a multi-target effect on the neuropathological process, memory and cognitive deficits of AD. Copyright © 2020 Zhao, Long, Ding, Jiang, Liu, Li, Liu, Peng, Wang, Feng and He.
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