ArticleMetallomics : integrated biometal science2020
Huntington's disease genotype suppresses global manganese-responsive processes in pre-manifest and manifest YAC128 mice.
Article in Metallomics : integrated biometal science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Differential impact of manganese on glutamate clearance, electroencephalography, and sleep in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- An iPSC-derived neuronal model reveals manganese's role in neuronal endocytosis, calcium flux and mitochondrial bioenergetics.iScience · 2025Article
- Homeostasis and metabolism of iron and other metal ions in neurodegenerative diseases.Signal transduction and targeted therapy · 2025Review
- A collaborative network analysis for the interpretation of transcriptomics data in Huntington's disease.Scientific reports · 2025Article
- Divalent metal content in diet affects severity of manganese toxicity in Drosophila.Biology open · 2024Article
- Widespread selenium deficiency in the brain of cases with Huntington's disease presents a new potential therapeutic target.EBioMedicine · 2023Article
- Consequences of Disturbing Manganese Homeostasis.International journal of molecular sciences · 2023Review
- Defective Mitochondrial Dynamics and Protein Degradation Pathways Underlie Cadmium-Induced Neurotoxicity and Cell Death in Huntington's Disease Striatal Cells.International journal of molecular sciences · 2023Article
- Acute manganese exposure impairs glutamatergic function in a young mouse model of Alzheimer's disease.Neurotoxicology · 2023Article
- Impaired XK recycling for importing manganese underlies striatal vulnerability in Huntington's disease.The Journal of cell biology · 2022Article
- Alterations in metal homeostasis occur prior to canonical markers in Huntington disease.Scientific reports · 2022Article
- Improving confidence in lipidomic annotations by incorporating empirical ion mobility regression analysis and chemical class prediction.Bioinformatics (Oxford, England) · 2022Article
- Manganese-induced hyperactivity and dopaminergic dysfunction depend on age, sex and YAC128 genotype.Pharmacology, biochemistry, and behavior · 2022Article
- Manganese-Induced Neurotoxicity through Impairment of Cross-Talk Pathways in Human Neuroblastoma Cell LineToxics · 2021Article
- YAC128 mouse model of Huntington disease is protected against subtle chronic manganese (Mn)-induced behavioral and neuropathological changes.Neurotoxicology · 2021Article
- Review
- Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update.International journal of molecular sciences · 2021Review
- The Impact of Environmental Factors on Monogenic Mendelian Diseases.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
Manganese (Mn) is an essential micronutrient required for the proper function of several enzymes. Accumulating evidence demonstrates a selective decrease of bioavailable Mn in vulnerable cell types of Huntington's Disease (HD), an inherited progressive neurodegenerative disorder with no cure. Amelioration of underlying pathophysiology, such as alterations in Mn-dependent biology, may be therapeutic. We therefore sought to investigate global Mn-dependent and Mn-responsive biology following various Mn exposures in a mouse model of HD. YAC128 and wildtype (WT) littermate control mice received one of three different Mn exposure paradigms by subcutaneous injection of 50 mg kg-1 MnCl2·4(H2O) across two distinct HD disease stages. "Pre-manifest" (12-week old mice) mice received either a single (1 injection) or week-long (3 injections) exposure of Mn or vehicle (H2O) and were sacrificed at the pre-manifest stage. "Manifest" (32-week old) mice were sacrificed following either a week-long Mn or vehicle exposure during the manifest stage, or a 20-week-long chronic (2× weekly injections) exposure that began in the pre-manifest stage. Tissue Mn, mRNA, protein, and metabolites were measured in the striatum, the brain region most sensitive to neurodegeneration in HD. Across all Mn exposure paradigms, pre-manifest YAC128 mice exhibited a suppressed response to transcriptional and protein changes and manifest YAC128 mice showed a suppressed metabolic response, despite equivalent elevations in whole striatal Mn. We conclude that YAC128 mice respond differentially to Mn compared to WT as measured by global transcriptional, translational, and metabolomic changes, suggesting an impairment in Mn homeostasis across two different disease stages in YAC128 mice.
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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 Socratic graph.