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Nontargeted metabolomics integrated with H NMR and LC-Q-TOF-MS/MS methods to depict a more comprehensive metabolic profile in response to chrysosplenetin and artemisinin co-treatment against artemisinin-sensitive and -resistant Plasmodium berghei K173.
Biomed Chromatogr
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Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou, China.
Our previous work revealed mutual and specific metabolites/pathways in artemisinin-sensitive and -resistant Plasmodium berghei K173-infected mice. In this study, we further investigated whether chrysosplenetin, a candidate chemical to prevent artemisinin resistance, can regulate these metabolites/pathways by integrating nontargeted metabolomics with H NMR and LC-Q-TOF-MS/MS spectrum. The nuclear magnetic resonance method generated specifically altered metabolites in response to co-treatment with chrysosplenetin, including: the products of glycolysis such as glucose, pyruvate, lactate and alanine; taurine, closely associated with liver injury; arginine and proline as essential amino acids for parasites; TMAO, a biomarker for dysbacteriosis and renal function; and tyrosine, which is used to generate levodopa and dopamine and may improve the torpor state of mice.
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Sci Rep
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Department of Cell Biology, Division of Host Defense Mechanism, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of extracellular amyloid-beta peptides (Aβ) resulting in senile plaques and intracellular hyperphosphorylated tau protein resulting in neurofibrillary tangles (NFTs). Mucuna beans (Mucuna pruriences (L.) DC.
View Article and Find Full Text PDFDiffuse Lewy body disease presenting as Parkinson's disease with progressive aphasia.
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Department of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.
Primary progressive aphasia (PPA) is a progressive language disorder often due to an underlying neurodegenerative disease. The most common pathologies associated with PPA include frontotemporal lobar degeneration (FTLD)-tau, FTLD-associated with transactivation response DNA-binding protein of 43 kDa (TDP-43) (FTLD-TDP), and Alzheimer's disease (AD). Accumulating evidence has suggested that Lewy body disease (LBD) can also be associated with PPA.
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School of Biosciences and Technology, VIT University, Vellore- 632014, Tamil Nadu, India.
Alzheimer's disease (AD) is supposed to stanch from inappropriate waving in the brain sections related to memory and perception. The incidence of AD in distressed person associated with an upsurge in the accumulation of amyloid plaque-rich senile plaques and neurofibrillary tangles in the brain. We hypothesize that a combination therapy provides a new treatment for AD.
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Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Inhibition of the accumulation of amyloid beta-peptide (Abeta) and the formation of beta-amyloid fibrils (fAbeta) from Abeta, as well as the destabilization of preformed fAbeta in the central nervous system would be attractive therapeutic targets for the treatment of Alzheimer's disease (AD). Many studies have demonstrated that oxidative damage plays a central role in AD pathogenesis, as well as Parkinson disease (PD). Among the antioxidant strategies proposed, increasing evidence points to the possibility of achieving neuroprotection by dopamine agonists, as well as monoamine oxidase B (MAO-B) inhibitors.
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