ArticleNeurobiology of disease2023
BDNF is altered in a brain-region specific manner and rescues deficits in Spinocerebellar Ataxia Type 1.
Article in Neurobiology of disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- TMEM206 gene knockout improves balance performance in SCA1 transgenic mice.IBRO neuroscience reports · 2025Article
- Article
- Intracerebellar upregulation of Rheb(S16H) ameliorates motor dysfunction in mice with SCA2.Acta pharmacologica Sinica · 2025Article
- Fingolimod Prevents Neuroinflammation but Has a Limited Effect on the Development of Ataxia in a Mouse Model for SCA1.International journal of molecular sciences · 2025Article
- Sex Differences in a Novel Mouse Model of Spinocerebellar Ataxia Type 1 (SCA1).International journal of molecular sciences · 2025Article
- Expanded ATXN1 alters transcription and calcium signaling in SCA1 human motor neurons differentiated from induced pluripotent stem cells.Neurobiology of disease · 2024Article
- Ablation of TrkB from Enkephalinergic Precursor-Derived Cerebellar Granule Cells Generates Ataxia.Biology · 2024Article
- Therapeutic Strategies for Spinocerebellar Ataxia Type 1.Biomolecules · 2023Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Spinocerebellar ataxia type 1 (SCA1) is an adult-onset, dominantly inherited neurodegenerative disease caused by the expanded polyQ tract in the protein ATAXIN1 (ATXN1) and characterized by progressive motor and cognitive impairments. There are no disease-modifying treatments or cures for SCA1. Brain-derived neurotrophic factor (BDNF) plays important role in cerebellar physiology and has shown therapeutic potential for cerebellar pathology in the transgenic mouse model of SCA1, ATXN1[82Q] line that overexpress mutant ATXN1 under a cerebellar Purkinje-cell-specific promoter. Here we demonstrate decreased expression of brain derived neurotrophic factor (BDNF) in the cerebellum and medulla of patients with SCA1. Early stages of disease seem most amenable to therapy. Thus, we next quantified Bdnf expression in Atxn1
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