Huntington's disease (HD) is an autosomal dominantly inherited disorder, caused by an expanded polyglutamine region of a protein called huntingtin. The excitotoxicity, oxidative damage and altered membrane transport may have an important role in the pathogenesis of HD. Probenecid is a non-selective inhibitor of multidrug resistance-associated proteins, but it also inhibits organic anion transporters. In this study, we examined the effects of probenecid on the survival, behaviour and immunohistochemical changes in the N171-82Q transgenic mouse model of HD. After probenecid administration, the duration of survival improved by 35%. The motor activity was significantly ameliorated as compared with the control transgenic group. Probenecid treatment significantly reduced the neuronal loss and the number of neuronal intranuclear aggregates. These results suggest that probenecid may exert a neuroprotective effect by increasing the membrane transport of protective compounds, and/or inhibiting the toxic compounds.
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http://dx.doi.org/10.1007/s00702-009-0253-6 | DOI Listing |
Curr Res Transl Med
January 2025
Department of Diabetology and Endocrinology, Hindu Mission Hospital, Tambaram, Chennai, 600045, Tamil Nadu, India.
Drug repurposing is a promising strategy for managing cardiovascular disease (CVD) in geriatric populations, offering efficient and cost-effective solutions. CVDs are prevalent across all age groups, with a significant increase in prevalence among geriatric populations. The middle-age period (40-65 years) is critical due to factors like obesity, sedentary lifestyle, and psychosocial stress.
View Article and Find Full Text PDFNeurogastroenterol Motil
January 2025
Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Background: Intestinal ischemia affects the functioning of the Enteric Nervous System (ENS). Pannexin-1 channel participates in cell communication and extracellular signaling. Probenecid (PB) is a pannexin-1 channel inhibitor, which can be a potential treatment for intestinal ischemia.
View Article and Find Full Text PDFJ Ethnopharmacol
December 2024
Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210008, China. Electronic address:
Ethnopharmacological Relevance: Banxia Xiexin Decoction (BXD) is a traditional herbal formulation with a bitter flavor that has a long-standing history of use in Asia for treating functional dyspepsia (FD). In traditional Chinese medicine, the bitter flavor is believed to play a critical role in the therapeutic activity of BXD. The ethnopharmacological properties of bitter plant extracts are closely associated with their anti-inflammatory effects, which may contribute to their efficacy in FD.
View Article and Find Full Text PDFClin Microbiol Infect
December 2024
Institute of Medical Microbiology and Virology, University Medical Center, Göttingen, Germany.
Background: Despite established antiviral therapy for herpes simplex virus, varicella zoster and cytomegalovirus encephalitis, the outcome remains poor.
Objectives: To assess pharmacokinetic (PK) and pharmacodynamic (PD) data of antiviral drugs in the central nervous system (CNS) to optimize the treatment of Herpesviridae encephalitis.
Sources: PUBMED search 1950 to September 2024, terms (1) "encephalitis" and ("HSV" or "VZV" or "CMV") or (2) cerebrospinal and ("(val)acyclovir" or "(val)ganciclovir" or "foscarnet" or "cidofovir").
Hum Mol Genet
December 2024
Children's Hospital of Eastern Ontario Research Institute, 401 Smyth Road, Ottawa K1H 8L1, Canada.
Riboflavin transporter deficiency (RTD) is a rare and progressive neurodegenerative disease resulting from the disruption of RFVT2- and RFVT3- mediated riboflavin transport caused by biallelic mutations in SLC52A2 and SLC52A3, respectively. The resulting impaired mitochondrial metabolism leads to sensorimotor neurodegeneration and symptoms including muscle weakness, respiratory difficulty, and sensorineural deafness. Although over 70% of patients with RTD improve following high-dose riboflavin supplementation, remaining patients either stabilise or continue to deteriorate.
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