ArticleFrontiers in molecular neuroscience2020
Quantification of Huntington's Disease Related Markers in the R6/2 Mouse Model.
Article in Frontiers in molecular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Role of aging‑related cytokines in neurodegenerative disease (Review).International journal of molecular medicine · 2026Review
- Neuroprotective Effects of Transplanted Induced Pluripotent Stem Cell-Derived Neural Precursors in Huntington's Disease Models.International journal of stem cells · 2026Article
- Fingolimod Effects on Motor Function and BDNF-TrkB Signaling in a Huntington's Mouse Model Are Disease-Stage-Dependent.International journal of molecular sciences · 2026Article
- 3D-AI mouse behavior analysis system has the capability to detect abnormalities in R6/1 model mice with Huntington's disease during the pre-symptomatic phase.Frontiers in psychiatry · 2026Article
- Evidence based molecular pathways, available drug targets, pre- clinical animal models and future disease modifying treatments of huntington's disease.Molecular biology reports · 2025Review
- Interventionally targeting somatic CAG expansions can be a rapid disease-modifying therapeutic avenue: Preclinical evidence.bioRxiv : the preprint server for biology · 2025Article
- Examination of Anti-Inflammatory Effects After Propionate Supplementation in the R6/2 Mouse Model of Huntington's Disease.International journal of molecular sciences · 2025Article
- The microbiota-gut-brain axis in Huntington's disease: pathogenic mechanisms and therapeutic targets.The FEBS journal · 2025Review
- Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain.Experimental neurology · 2024Review
- Neuroprotection by ADAM10 inhibition requires TrkB signaling in the Huntington's disease hippocampus.Cellular and molecular life sciences : CMLS · 2024Article
- Deregulated Transcriptome as a Platform for Adrenal Huntington's Disease-Related Pathology.International journal of molecular sciences · 2024Article
- A Novel Huntington's Disease Assessment Platform to Support Future Drug Discovery and Development.International journal of molecular sciences · 2022Article
- Postnatal Conditional Deletion ofBiomedicines · 2022Article
- Neuroinflammation in Huntington's disease: From animal models to clinical therapeutics.Frontiers in immunology · 2022Review
- Olfactory Dysfunction in Huntington's Disease.Journal of Huntington's disease · 2021Review
- Evaluation of Neuropathological Features in the SOD1-G93A Low Copy Number Transgenic Mouse Model of Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is caused by an expansion of CAG triplets in the huntingtin gene, leading to severe neuropathological changes that result in a devasting and lethal phenotype. Neurodegeneration in HD begins in the striatum and spreads to other brain regions such as cortex and hippocampus, causing motor and cognitive dysfunctions. To understand the signaling pathways involved in HD, animal models that mimic the human pathology are used. The R6/2 mouse as model of HD was already shown to present major neuropathological changes in the caudate putamen and other brain regions, but recently established biomarkers in HD patients were yet not analyzed in these mice. We therefore performed an in-depth analysis of R6/2 mice to establish new and highly translational readouts focusing on Ctip2 as biological marker for motor system-related neurons and translocator protein (TSPO) as a promising readout for early neuroinflammation. Our results validate already shown pathologies like mutant huntingtin aggregates, ubiquitination, and brain atrophy, but also provide evidence for decreased tyrosine hydroxylase and Ctip2 levels as indicators of a disturbed motor system, while vesicular acetyl choline transporter levels as marker for the cholinergic system barely change. Additionally, increased astrocytosis and activated microglia were observed by GFAP, Iba1 and TSPO labeling, illustrating, that TSPO is a more sensitive marker for early neuroinflammation compared to GFAP and Iba1. Our results thus demonstrate a high sensitivity and translational value of Ctip2 and TSPO as new marker for the preclinical evaluation of new compounds in the R6/2 mouse model of HD.
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