ArticlePloS one2010
Genistein improves neuropathology and corrects behaviour in a mouse model of neurodegenerative metabolic disease.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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The trial behind it
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Who cites it
69 citing papers in PubMed, 138 citations in OpenAlex.
- Genistein stimulates insulin sensitivity through gut microbiota reshaping and skeletal muscle AMPK activation in obese subjects.BMJ open diabetes research & care · 2020Trial
- Genistein supplementation in patients affected by Sanfilippo disease.Journal of inherited metabolic disease · 2011Trial
- Two-year follow-up of Sanfilippo Disease patients treated with a genistein-rich isoflavone extract: assessment of effects on cognitive functions and general status of patients.Medical science monitor : international medical journal of experimental and clinical research · 2011Trial
- Advances in Therapies for Mucopolysaccharidoses.Current issues in molecular biology · 2026Review
- Short-Term Oral Spermidine Supplementation Modifies Aspects of Neurodegenerative Disease in Flies and Mice With MPS III.Journal of inherited metabolic disease · 2026Article
- TFEB, FOXO3 and TLR4 in resveratrol-induced autophagy in a mucopolysaccharidosis IIIB mouse model.Experimental & molecular medicine · 2026Article
- The use of genistein and ambroxol may be an effective approach in correcting cellular dysfunctions of mucopolysaccharidosis-plus syndrome.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Neuroinflammation as a Novel Therapeutic Frontier for Sanfilippo Syndrome.Children (Basel, Switzerland) · 2025Review
- Mucopolysaccharidoses-What Clinicians Need to Know: A Clinical, Biochemical, and Molecular Overview.Biomolecules · 2025Review
- Heparan sulfate binding protein treatment ameliorates neuropathology and behavioral abnormalities in mucopolysaccharidosis IIIB mice.Cell death discovery · 2025Article
- Current Concepts in the Management of Sanfilippo Syndrome (MPS III): A Narrative Review.Cureus · 2024Review
- Efficacy of a Combination Therapy with Laronidase and Genistein in Treating Mucopolysaccharidosis Type I in a Mouse Model.International journal of molecular sciences · 2024Article
- Article
- Genistein improves renal disease in a mouse model of nephropathic cystinosis: a comparison study with cysteamine.Human molecular genetics · 2023Article
- Article
- Activities of (Poly)phenolic Antioxidants and Other Natural Autophagy Modulators in the Treatment of Sanfilippo Disease: Remarkable Efficacy of Resveratrol in Cellular and Animal Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Mucopolysaccharidoses: Cellular Consequences of Glycosaminoglycans Accumulation and Potential Targets.International journal of molecular sciences · 2022Review
- Murine Fibroblasts and Primary Hepatocytes as Tools When Studying the Efficacy of Potential Therapies for Mucopolysaccharidosis Type I.International journal of molecular sciences · 2022Article
- Innate Immunity in Mucopolysaccharide Diseases.International journal of molecular sciences · 2022Review
- Cellular and Gene Expression Response to the Combination of Genistein and Kaempferol in the Treatment of Mucopolysaccharidosis Type I.International journal of molecular sciences · 2022Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeurodegenerative metabolic disorders such as mucopolysaccharidosis IIIB (MPSIIIB or Sanfilippo disease) accumulate undegraded substrates in the brain and are often unresponsive to enzyme replacement treatments due to the impermeability of the blood brain barrier to enzyme. MPSIIIB is characterised by behavioural difficulties, cognitive and later motor decline, with death in the second decade of life. Most of these neurodegenerative lysosomal storage diseases lack effective treatments. We recently described significant reductions of accumulated heparan sulphate substrate in liver of a mouse model of MPSIIIB using the tyrosine kinase inhibitor genistein. METHODOLOGY/PRINCIPAL
findingsWe report here that high doses of genistein aglycone, given continuously over a 9 month period to MPSIIIB mice, significantly reduce lysosomal storage, heparan sulphate substrate and neuroinflammation in the cerebral cortex and hippocampus, resulting in correction of the behavioural defects observed. Improvements in synaptic vesicle protein expression and secondary storage in the cerebral cortex were also observed. CONCLUSIONS/SIGNIFICANCE: Genistein may prove useful as a substrate reduction agent to delay clinical onset of MPSIIIB and, due to its multimodal action, may provide a treatment adjunct for several other neurodegenerative metabolic diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.