Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Background: Pridopidine is a novel drug that helps stabilize psychomotor function in patients with Huntington's disease (HD) by activating the cortical glutamate pathway. It promises to achieve the unmet needs of current therapies of HD without worsening other symptoms.
Objective: To review the literature discussing the efficacy of pridopidine in alleviating motor symptoms and its safety in patients with HD.
Methods: We searched Scopus, Web of Science, the Cochrane Library, Wiley, and PubMed for randomized controlled trials (RCTs) of pridopidine on HD. Data from eligible studies were extracted and pooled as mean differences for efficacy and risk ratios (RRs) for safety using RevMan software version 5.3.
Results: A total of 4 relevant RCTs with 1130 patients were selected (816 in the pridopidine group and 314 in the placebo group). The pooled effect size favored pridopidine over placebo insignificantly in the Unified Huntington's Disease Rating Scale Total Motor Score (mean difference [MD], -0.93; 95% confidence interval [CI], -2.01 to 0.14; = 0.09), whereas the effect size of 3 studies significantly favored pridopidine over placebo in the Unified Huntington's Disease Rating Scale Modified Motor Score (MD, -0.81; 95% CI, -1.48 to -0.13; = 0.02). Pridopidine generally was well tolerated. None of the adverse effects were considerably higher in the case of pridopidine compared with placebo in overall adverse events (RR, 1.03; 95% CI, 0.94-1.13; = 0.49) and serious adverse events (RR, 1.62; 95% CI, 0.88-2.99; = 0.12).
Conclusion: The effects of pridopidine on motor functions (especially voluntary movements) in patients with HD are encouraging and provide a good safety profile that motivates further clinical trials on patients to confirm its effectiveness and safety.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8721839 | PMC |
| http://dx.doi.org/10.1002/mdc3.13357 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Prevalence and risk factors of metabolic dysfunction-associated steatotic liver disease in patients with inflammatory bowel disease.
Eur J Gastroenterol Hepatol
September 2025
Division of Gastroenterology and Hepatology, Department of Internal Medicine, School of Medicine, The University of Jordan, Jordan University Hospital.
Aim: The purpose of our study was to evaluate the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) and its associated risk factors in patients with inflammatory bowel disease (IBD).
Methods: This was a retrospective chart review of patients who underwent treatment for IBD at Jordan University Hospital between January 2013 and 2022. Case finding methods and clinical chart reviews were used to evaluate the clinical profile of patients with IBD.
Global transcriptional analysis of human FHs 74 Int intestinal epithelial cells after exposure to advanced glycation end products.
PLoS One
September 2025
Institute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology & Immunology, Medical University of Vienna, Vienna, Austria.
Advanced glycation end products (AGEs) and reactive intermediates, such as methylglyoxal, are formed during thermal processing of foods and have been implicated in the pathogenesis of a series of chronic inflammatory diseases. AGEs are thought to directly interact with the intestinal epithelium upon ingestion of thermally processed foods, but their effects on intestinal epithelial cells are poorly understood. This study investigated transcriptomic changes in human intestinal epithelial FHs 74 Int cells after exposure to AGE-modified human serum proteins (AGE-HS), S100A12, a known RAGE ligand, and unmodified human serum proteins (HS).
View Article and Find Full Text PDFPotential repurposing of lapatinib and pazopanib as neuroprotective agents in a rat model of Huntington's disease.
Inflammopharmacology
September 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA University), Giza, Egypt.
The neuroprotective potential of tyrosine kinase inhibitors (TKIs), potent anticancer drugs, was verified against various neurodegenerative insults, but not Huntington's disease (HD). These promising outcomes were due to their ability to modulate various intracellular signalling pathways. Hence, the current study aimed to evaluate the neuroprotective effects of lapatinib and pazopanib in the 3-nitropropionic (3-NP)-induced HD model in rats.
View Article and Find Full Text PDFNovel small molecule derivatives improve survivability in the cellular model of Huntington's disease improving mitochondrial fusion.
RSC Med Chem
August 2025
Department of Biological Science, Birla Institute of Technology and Science, Pilani Hyderabad Campus, Jawahar Nagar, Kapra Mandal, Medchal District Telangana 500078 India
Mitochondrial dysfunction is one of the primary cellular conditions involved in developing Huntington's disease (HD) pathophysiology. The accumulation of mutant huntingtin protein with abnormal PolyQ repeats resulted in the death of striatal neurons with enhanced mitochondrial fragmentation. In search of neuroprotective molecules against HD conditions, we synthesized a set of isoxazole-based small molecules to screen their suitability as beneficial chemicals improving mitochondrial health.
View Article and Find Full Text PDFMutant huntingtin exon 1 protein detected in mouse brain with neoepitope antibody: effects of CAG repeat expansion, MutS Homolog 3 silencing and aggregation.
Brain Commun
August 2025
Department of Neurology, Massachusetts General Hospital, Charlestown, MA 02129, USA.
was identified in human and mouse Huntington's disease brain as the pathogenic exon 1 mRNA generated from aberrant splicing between exon 1 and 2 of that contributes to aggregate formation and neuronal dysfunction. Detection of the huntingtin exon 1 protein (HTT1a) has been accomplished with Meso Scale Discovery, Homogeneous Time Resolved Fluorescence and immunoprecipitation assays in Huntington's disease knock-in mice, but direct detection in homogenates by gel electrophoresis and western blot assay has been lacking. Subcellular fractions prepared from mouse and human Huntington's disease brain were separated by gel electrophoresis and probed by western blot with neoepitope monoclonal antibodies 1B12 and 11G2 directed to the C-terminal eight residues of HTT1a.
View Article and Find Full Text PDF