The concentration of the endogenous excitotoxin quinolinic acid was determined in the cerebrospinal fluid of drug-free patients suffering from Huntington's disease or schizophrenia (control group). In both diseases, quinolinic acid concentrations were highly variable (less than 4-48 nM) but the mean levels for each disease group were not significantly different from each other or from the quinolinic acid concentration of normal cerebrospinal fluid. Analysis of steady-state cerebrospinal fluid quinolinic acid concentration is unlikely to be of value as a diagnostic tool in Huntington's disease.
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http://dx.doi.org/10.1002/ana.410240417 | DOI Listing |
Colorectal cancer (CRC) is a prevalent and deadly disease, necessitating the exploration of novel therapeutic strategies. Traditional chemotherapy often encounters drug resistance and adverse side effects, highlighting the need for alternative approaches. , a plant rich in phytochemical constituents, was investigated for its potential as an anticancer agent against colorectal cancer (CRC).
View Article and Find Full Text PDFRapid Commun Mass Spectrom
March 2025
Department of Cardiology, Xinjiang Traditional Chinese Medicine Hospital, Xinjiang, China.
Exp Neurol
January 2025
Laboratory of Neurodegenerative Diseases and Neuroinjury Diseases, Wuxi, School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China; MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu 214122, China. Electronic address:
Abnormal tryptophan metabolism is closely linked with neurological disorders. Research has shown that indoleamine 2,3-dioxygenase 1 (IDO-1), the first rate-limiting enzyme in tryptophan degradation, is upregulated in Parkinson's disease (PD). However, the precise role of IDO-1 in PD pathogenesis remains elusive.
View Article and Find Full Text PDFHepatol Commun
December 2024
Macquarie Medicine School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney, Australia.
Background: HE is a neuropsychiatric complication of liver disease characterized by systemic elevation in ammonia and proinflammatory cytokines. These neurotoxins cross the blood-brain barrier and cause neuroinflammation, which can activate the kynurenine pathway (KP). This results in dysregulated production of neuroactive KP metabolites, such as quinolinic acid, which is known to cause astrocyte and neuronal death.
View Article and Find Full Text PDFToxics
December 2024
Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China.
Methamphetamine (METH) abuse disrupts the homeostasis of neurotransmitter (NT) metabolism, contributing to a wide range of neurological and psychological disorders. However, the specific effects of METH on NT metabolism, particularly for the tryptophan (TRP) and tyrosine (TYR) metabolic pathways, remain poorly understood. In this study, serum samples from 78 METH abusers and 79 healthy controls were analyzed using Ultra-High-Performance Liquid Chromatography with Tandem Mass Spectrometry (UHPLC-MS/MS).
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