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2,052 results on '"Huang, Xu-Feng"'

17. Butyrate ameliorates quinolinic acid-induced cognitive decline in obesity models

Author

Ge, Xing, Zheng, Mingxuan, Hu, Minmin, Fang, Xiaoli, Geng, Deqin, Liu, Sha, Wang, Li, Zhang, Jun, Guan, Li, Zheng, Peng, Xie, Yuanyi, Pan, Wei, Zhou, Menglu, Zhou, Limian, Tang, Renxian, Zheng, Kuiyang, Yu, Yinghua, and Huang, Xu-Feng

Subjects
Quinolinic acid -- Complications and side effects, Obesity -- Complications and side effects -- Models, Fatty acids -- Health aspects, Cognition disorders -- Care and treatment -- Models -- Development and progression, Health care industry
Abstract

Obesity is a risk factor for neurodegenerative disease associated with cognitive dysfunction, including Alzheimer's disease. Low-grade inflammation is common in obesity, but the mechanism between inflammation and cognitive impairment in obesity is unclear. Accumulative evidence shows that quinolinic acid (QA), a neuroinflammatory neurotoxin, is involved in the pathogenesis of neurodegenerative processes. We investigated the role of QA in obesity-induced cognitive impairment and the beneficial effect of butyrate in counteracting impairments of cognition, neural morphology, and signaling. We show that in human obesity, there was a negative relationship between serum QA levels and cognitive function and decreased cortical gray matter. Diet-induced obese mice had increased QA levels in the cortex associated with cognitive impairment. At single-cell resolution, we confirmed that QA impaired neurons, altered the dendritic spine's intracellular signal, and reduced brain-derived neurotrophic factor (BDNF) levels. Using Caenorhabditis elegans models, QA induced dopaminergic and glutamatergic neuron lesions. Importantly, the gut microbiota metabolite butyrate was able to counteract those alterations, including cognitive impairment, neuronal spine loss, and BDNF reduction in both in vivo and in vitro studies. Finally, we show that butyrate prevented QA-induced BDNF reductions by epigenetic enhancement of H3K18ac at BDNF promoters. These findings suggest that increased QA is associated with cognitive decline in obesity and that butyrate alleviates neurodegeneration., Introduction Obesity is a growing health concern that has increased in prevalence worldwide in the past 50 years, reaching pandemic levels (1). Obesity is also associated with cognitive dysfunction and [...]

Published
2023
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33. Investigating the Therapeutic Potential of Plants and Plant-Based Medicines: Relevance to Antioxidant and Neuroprotective Effects

Author

May, Naomi, primary, de Sousa Alves Neri, Julianna Lys, additional, Clunas, Helen, additional, Shi, Jiahua, additional, Parkes, Ella, additional, Dongol, Anjila, additional, Wang, Zhizhen, additional, Jimenez Naranjo, Carlos, additional, Yu, Yinghua, additional, Huang, Xu-Feng, additional, Charlton, Karen, additional, and Weston-Green, Katrina, additional

Published
2023
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42. A postmortem analysis of NMDA ionotropic and group 1 metabotropic glutamate receptors in the nucleus accumbens in schizophrenia

Author

Lum, Jeremy S., Millard, Samuel J., Huang, Xu-Feng, Ooi, Lezanne, and Newell, Kelly A.

Subjects
N-methyl-D-aspartate -- Physiological aspects, Schizophrenia -- Physiological aspects, Nucleus accumbens -- Physiological aspects, Health, Psychology and mental health
Abstract

Background: The nucleus accumbens (NAcc) has been implicated in the pathology and treatment of schizophrenia. Recent postmortem evidence suggests a hyperglutamatergic state in the NAcc. With the present study we aimed to explore possible glutamatergic alterations in the NAcc of a large schizophrenia cohort. Methods: We performed immunoblots on postmortem NAcc samples from 30 individuals who had schizophrenia and 30 matched controls. We examined the protein expression of primary glutamatergic receptors, including the W-methyl-D-aspartate (NMDA) receptor (NR1, NR2A and NR2B subunits) and the group 1 metabotropic glutamate receptor (mGluR1 and mGluR5; dimeric and monomeric forms). In addition, we measured the group 1 mGluR endogenous regulators, neurochondrin and Homer1b/c, which have recently been implicated in the pathophysiology of schizophrenia. Results: Protein levels of glutamatergic receptors and endogenous regulators were not significantly different between the controls and individuals who had schizophrenia. Furthermore, mGluR5, but not mGluR1, showed a positive association with NMDA receptor subunits, suggesting differential interactions between these receptors in this brain region. Limitations: Investigation of these proteins in antipsychotic-naive individuals, in addition to the subregions of the NAcc and subcellular fractions, will strengthen future studies. Conclusion: The present study does not provide evidence for glutamatergic abnormalities within the NAcc of individuals with schizophrenia. Taken together with the results of previous studies, these findings suggest NMDA receptors and group 1 mGluRs are altered in a brain region-dependent manner in individuals with schizophrenia. The differential associations between mGluRI, mGluR5 and NMDA receptors observed in this study warrant further research into the interactions of these proteins and the implications for the therapeutic and adverse effect profile of glutamatergic-based novel therapeutics., Introduction The nucleus accumbens (NAcc), a major component of the ventral striatum, is believed to play a large role in the pathology of schizophrenia; however, there has been little direct [...]

Published
2018
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