ArticleCell2019
Loss of Ataxin-1 Potentiates Alzheimer's Pathogenesis by Elevating Cerebral BACE1 Transcription.
Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
42 citing papers in PubMed, 65 citations in OpenAlex.
- Zebrafish knockout models of atxn1a, atxn1b, and atxn1l reveal distinct and shared phenotypic and transcriptomic alterations.Human molecular genetics · 2026Article
- Functional divergence of Capicua isoforms explains differential tissue vulnerability in neurological disease.Genes & development · 2026Article
- Multiomics Profiling During Autoimmune Demyelination Highlights a Complex Regulatory Role for Ataxin-1 in B Cells.Annals of the New York Academy of Sciences · 2026Article
- Oligodendrocyte dysfunction contributes to motor deficits and Purkinje cell axonopathy in spinocerebellar ataxia type 1.The Journal of clinical investigation · 2026Article
- Brain-targeted delivery of siRNA via non-viral delivery systems, the therapeutic strategy for Alzheimer's disease-Unveiling challenges and prospects.International journal of pharmaceutics: X · 2026Review
- Conditional deletion of the multiple sclerosis susceptibility gene ATXN1 identifies cell-autonomous effects in the B-cell compartment.The FEBS journal · 2026Article
- Targeted methylation of cg24067911 suppresses colorectal cancer metastasis through BCL6-ATXN1-CDH1 axis.Oncogene · 2026Article
- Epigenetic and transcriptomic alterations precede amyloidosis in the Alzheimer's disease AppScientific reports · 2025Article
- Functional divergence of Capicua isoforms explains differential tissue vulnerability in neurological disease.bioRxiv : the preprint server for biology · 2025Article
- Identification of Splicing Regulatory Activity of ATXN1 and Its Associated Domains.Biomolecules · 2025Article
- Drofenine as a Kv2.1 inhibitor alleviated AD-like pathology in mice through AActa pharmaceutica Sinica. B · 2025Article
- CRISPR-Cas9-directed gene therapy for spinocerebellar ataxia type 1.Molecular therapy. Nucleic acids · 2024Article
- Current Insights of Nanocarrier-Mediated Gene Therapeutics to Treat Potential Impairment of Amyloid Beta Protein and Tau Protein in Alzheimer's Disease.Molecular neurobiology · 2024Review
- Nanotechnology-based gene therapy as a credible tool in the treatment of Alzheimer's disease.Neural regeneration research · 2023Review
- Therapeutic Strategies for Spinocerebellar Ataxia Type 1.Biomolecules · 2023Review
- BDNF is altered in a brain-region specific manner and rescues deficits in Spinocerebellar Ataxia Type 1.Neurobiology of disease · 2023Article
- DSCR1 deficiency ameliorates the Aβ pathology of Alzheimer's disease by enhancing microglial activity.Life science alliance · 2023Article
- Review
- Six mitophagy-related hub genes as peripheral blood biomarkers of Alzheimer's disease and their immune cell infiltration correlation.Frontiers in neuroscience · 2023Article
- Suppressing gain-of-function proteins via CRISPR/Cas9 system in SCA1 cells.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 1 country.
Funding
Abstract
Expansion of CAG trinucleotide repeats in ATXN1 causes spinocerebellar ataxia type 1 (SCA1), a neurodegenerative disease that impairs coordination and cognition. While ATXN1 is associated with increased Alzheimer's disease (AD) risk, CAG repeat number in AD patients is not changed. Here, we investigated the consequences of ataxin-1 loss of function and discovered that knockout of Atxn1 reduced CIC-ETV4/5-mediated inhibition of Bace1 transcription, leading to increased BACE1 levels and enhanced amyloidogenic cleavage of APP, selectively in AD-vulnerable brain regions. Elevated BACE1 expression exacerbated Aβ deposition and gliosis in AD mouse models and impaired hippocampal neurogenesis and olfactory axonal targeting. In SCA1 mice, polyglutamine-expanded mutant ataxin-1 led to the increase of BACE1 post-transcriptionally, both in cerebrum and cerebellum, and caused axonal-targeting deficit and neurodegeneration in the hippocampal CA2 region. These findings suggest that loss of ataxin-1 elevates BACE1 expression and Aβ pathology, rendering it a potential contributor to AD risk and pathogenesis.
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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.