ArticleNeurobiology of disease2015
Selective reduction of striatal mature BDNF without induction of proBDNF in the zQ175 mouse model of Huntington's disease.
Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Oligodendroglial Mutant Huntingtin Contributes to Neuroinflammation in Huntington's Disease Mice.Neuroscience bulletin · 2026Article
- Neuroprotective Effects of Transplanted Induced Pluripotent Stem Cell-Derived Neural Precursors in Huntington's Disease Models.International journal of stem cells · 2026Article
- Taming the "death receptor": translating the first-in-class p75Journal of translational medicine · 2026Review
- The role of oligodendroglial dysfunction in Huntington's disease.Journal of Huntington's disease · 2025Review
- Brain-Derived Neurotrophic Factor (BDNF) in Huntington's Disease: Neurobiology and Therapeutic Potential.Current neuropharmacology · 2025Review
- Nebulization of low-dose aspirin ameliorates Huntington's pathology in N171-82Q transgenic mice.NeuroImmune pharmacology and therapeutics · 2024Article
- Brain-Derived Neurotrophic Factor Dysregulation as an Essential Pathological Feature in Huntington's Disease: Mechanisms and Potential Therapeutics.Biomedicines · 2023Review
- Article
- Recent Advances on the Role of Brain-Derived Neurotrophic Factor (BDNF) in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Brain-derived neurotrophic factor in cerebrospinal fluid and plasma is not a biomarker for Huntington's disease.Scientific reports · 2021Article
- Dorsolateral Striatal proBDNF Improves Reversal Learning by Enhancing Coordination of Neural Activity in Rats.Molecular neurobiology · 2020Article
- Differential regulation of Kidins220 isoforms in Huntington's disease.Brain pathology (Zurich, Switzerland) · 2020Article
- ATAT1 regulates forebrain development and stress-induced tubulin hyperacetylation.Cellular and molecular life sciences : CMLS · 2019Article
- Metformin treatment reduces motor and neuropsychiatric phenotypes in the zQ175 mouse model of Huntington disease.Experimental & molecular medicine · 2019Article
- Early Downregulation of p75Molecular neurobiology · 2019Article
- Targeted Depletion of Primary Cilia in Dopaminoceptive Neurons in a Preclinical Mouse Model of Huntington's Disease.Frontiers in cellular neuroscience · 2019Article
- The Role of Hypothalamic Pathology for Non-Motor Features of Huntington's Disease.Journal of Huntington's disease · 2019Review
- Actions of Brain-Derived Neurotrophin Factor in the Neurogenesis and Neuronal Function, and Its Involvement in the Pathophysiology of Brain Diseases.International journal of molecular sciences · 2018Review
- TSPO-PET imaging using [18F]PBR06 is a potential translatable biomarker for treatment response in Huntington's disease: preclinical evidence with the p75NTR ligand LM11A-31.Human molecular genetics · 2018Article
- Low pH-induced conformational change and dimerization of sortilin triggers endocytosed ligand release.Nature communications · 2017Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Huntington's disease (HD) is a neurodegenerative disorder characterized by massive loss of medium spiny neurons in the striatum. However, the mechanisms by which mutant huntingtin leads to this selective neuronal death remain incompletely understood. Brain-derived neurotrophic factor (BDNF) has been shown to be neuroprotective on HD striatal neurons both in vitro and in vivo. ProBDNF, the precursor of mature BDNF (mBDNF), also can be secreted but promotes apoptosis of neurons expressing p75(NTR) and sortilin receptors. Although a reduction of total striatal BDNF protein has been reported in HD patients and mouse models, it remains unclear whether conversion of proBDNF to mBDNF is altered in HD, and whether the proBDNF receptors, p75(NTR) and sortilin are dysregulated, leading to impaired striatal neuron survival. To test these hypotheses, we generated bdnf-HA knock-in (KI) mice on the zQ175 HD background to accurately quantitate the levels of both proBDNF and mBDNF in the HD striatum. In aged zQ175 HD mice, we observed a significant loss of mBDNF and decreased TrkB activation, but no increase of proBDNF or p75(NTR) levels either in the sensorimotor cortex or the striatum. However, immunoreactivities of p75(NTR) and sortilin receptor are both increased in immature striatal oligodendrocytes, which associate with significant myelin defects in the HD striatum. Taken together, the present study indicates that diminished mature BDNF trophic signaling through the TrkB receptor, rather than an induction in proBDNF, is a main contributing factor to the vulnerability of striatal neurons in the zQ175 HD mouse model.
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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.