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Strength training when pregnant influences hippocampal plasticity but not physique development in neonatal test subjects.
TGM6 encodes transglutaminase 6, which catalyzes the covalent crosslinking of proteins through transamination reactions. Variants in TGM6 have been identified as the cause of spinocerebellar ataxia type 35. However, we found 12 TGM6 variants of low frequency among 308 patients with Parkinson's disease using next-generation sequencing technologies and multiple ligation-dependent probe amplification, including two variants TGM6 p.R111C and p.L517W, which have been reported to affect functions of transglutaminase 6 in spinocerebellar ataxia type 35 cases. The characteristics of these TGM6 carriers were summarized. To clarify the role of TGM6 variants in Parkinson's disease, we constructed the plasmids of wild-type TGM6 and TGM6 p.R111C, p.P359L, p.L517W to transfect A53T-SH-SY5Y cells and conducted transglutaminase assay, western blots, immunofluorescence, and cell viability assay. Results revealed that the distribution and expression levels of transglutaminase 6 were not affected by TGM6 variants. BGB-8035 supplier However, the variants showed lower transglutaminase activity than wild-type transglutaminase 6. The overexpression of wild-type TGM6 was proved to relieve the cell damage, down-regulate the level of α-synuclein and enhance autophagy. These effects were weakened in cells transfected with mutant TGM6 plasmids. Our results suggested that there may be some relationship between TGM6 and Parkinson's disease. TGM6 carriers in Parkinson's disease patients presented with typical parkinsonism but progressed slower. The high expression level of wild-type transglutaminase 6 may protect cells by decreasing α-synuclein and enhancing autophagy. © 2020 Chen et al. Published by IMR press.Depression is a common mental health disorder that can impair normal functions, cause distress, and adversely affect the quality of life. Cognitive impairment is considered one of the characteristics of major depression disorders-related dysfunction, and it has received attention in the treatment of major depressive disorders. To investigated the mechanisms underlying depression-induced cognitive disorders, we selected a rodent model of chronic unpredictable mild stress and used liquid chromatography/mass spectrometry-based metabolomics of sera. Behavioral tests, including the sucrose preference test and open field test, revealed that model rats developed depression-like symptoms in the sixth week of the chronic unpredictable mild stress period. Rats of the model group exhibited significant cognitive changes in the Morris water maze test in the tenth week of the period. Tau phosphorylation and decreased levels of postsynaptic density-95 and synaptophysin were observed in the rodent brains by the tenth week. These results suggest that rodents developed cognitive impairment in the tenth week of the period, while serum metabonomic showed that glycerophospholipid metabolism is the most relevant pathway to reveal the mechanism of depression-induced cognitive impairment. The disorders of lipid metabolism caused by the increased cholesterol efflux and reduced reuptake could be one of the mechanisms of depression-induced cognitive disorders. However, the relationship between cholesterol efflux in the brain and elevated serum cholesterol needs further research. © 2020 Ye et al. Published by IMR press.Post-traumatic hydrocephalus is a common complication secondary to traumatic brain injury. It can cause cerebral metabolic impairment and dysfunction. Therefore, timely treatment with shunt implantation is necessary. However, the outcomes of shunt surgery in patients with post-traumatic hydrocephalus combined with disturbance of consciousness are doubtful. The objective was to develop a predictive model that uses the information available before surgery to predict the outcome of shunt implantation in such patients. Retrospectively collected data were used to develop a clinical prediction model. The model was derived from 59 patients using logistic regression analysis, and then it was evaluated by the area under the receiver operating characteristic curve and Hosmer-Lemshow test. A validation cohort verified the model. Four independent predictors were identified age less then 50 years, mild hydrocephalus, Glasgow Coma Scale scores 9-12 at the time of injury, and time interval from trauma to shunting less then 3 months. We calculated the total score and defined the patients into three groups low-probability (0-10 points), medium-probability (11-16 points), and high-probability (17-30 points). The rates of improved outcomes in the three groups were 14.3%, 52.6%, and 94.7%, respectively (P less then 0.0001). The correlative rates of the validation cohort were 21.4%, 54.5%, and 85.7%. The prognostic model showed good discrimination (area under the receiver operating characteristic curve = 0.869) and calibration (Hosmer-Lemshow test, P = 0.391). The developed predictive model can identify patients with post-traumatic hydrocephalus combined with disturbance of consciousness who can benefit from shunt implantation. Therefore, our prognostic model can predict the outcomes of patients with post-traumatic hydrocephalus and disturbance of consciousness after shunt surgery. © 2020 Wang et al. Published by IMR press.The neuroprotective role of Fructus Broussonetiae in a model of chronic cerebral hypoperfusion with cognitive decline was focused on neural plasticity and microglia/macrophage polarization. Chronic cerebral hypoperfusion was induced by bilateral common carotid artery ligation. Fructus Broussonetiae shortened escape latency and added the number of platform crossings of rats, up-regulated the expression of synaptophysin in the gray matter and increased myelin basic protein expression in the white matter. Further mechanistic experiments were conducted to examine microglia activation and M1/M2 polarization. It was shown that Fructus Broussonetiae reduced the activation of microglia revealed by decreased expression of ionized calcium-binding adapter molecule-1, inhibited M1 polarization of microglia and improved microglial M2 polarization shown by down-regulated the expression of inducible nitric oxide synthase and Fc fragment of IgG receptor IIIa and up-regulated the expression of arginase-1. In conclusion, the Chinese herb Fructus Broussonetiae can improve cognitive function following chronic cerebral hypoperfusion by down-regulating the activation of microglia, inhibiting microglial M1 polarization, and improving neural plasticity.
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