ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Single-nucleus analysis reveals oxidative stress in Down syndrome basal forebrain neurons at birth.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- A lifespan staging model of basal forebrain cholinergic vulnerability.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- A single-cell multiomic analysis identifies molecular and gene-regulatory mechanisms dysregulated in developing Down syndrome neocortex.Science (New York, N.Y.) · 2026Article
- Use of anti-amyloid-β monoclonal antibodies in persons with Down syndrome Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Genome-wide cell type-specific and sex-specific transcriptional dysregulation in the islet of Langerhans underlies islet dysfunction in Down syndrome-related diabetes.bioRxiv : the preprint server for biology · 2026Article
- The cholinergic system exerts opposing effects on memory at different stages of disease progression in Alzheimer's and Down syndrome model systems.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Dual-Omics Mapping of Tinnitus Phenotype Transition in Noise-Exposed Auditory Cortex.Cellular and molecular neurobiology · 2025Article
- Development of Molecular Neuropathology in Down Syndrome across the Lifespan.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Warp analysis research pipelines: cloud-optimized workflows for biological data processing and reproducible analysis.Bioinformatics (Oxford, England) · 2025Article
- Single-nucleus analysis reveals oxidative stress in Down syndrome basal forebrain neurons at birth.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
Corrections and comments
- Erratum issued
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Authors and funding
12 authors.
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Abstract
introductionBasal forebrain cholinergic neurons (BFCNs) are integral to learning, attention, and memory, and are prone to degeneration in Down syndrome (DS), Alzheimer's disease, and other neurodegenerative diseases. However, the mechanisms that lead to the degeneration of these neurons are not known.
methodsSingle-nucleus gene expression and Assay for Transposase-Accessible Chromatin (ATAC) sequencing were performed on postmortem human basal forebrain from unaffected control and DS tissue samples at 0-2 years of age (n = 4 each).
resultsSequencing analysis of postmortem human basal forebrain identifies gene expression differences in DS early in life. Genes encoding proteins associated with energy metabolism pathways, specifically oxidative phosphorylation and glycolysis, and genes encoding antioxidant enzymes are upregulated in DS BFCNs. DISCUSSION: Multiomic analyses reveal that energy metabolism may be disrupted in DS BFCNs by birth. Increased oxidative phosphorylation and the accumulation of reactive oxygen species byproducts may be early contributors to DS BFCN neurodegeneration. HIGHLIGHTS: First multiomic gene expression and ATAC analysis of human basal forebrain. Basal forebrain pathology in DS begins by birth. Cell type proportions are altered in early postnatal DS basal forebrain. Gene expression suggests dysregulated energy metabolism in DS BFCNs. Genes encoding oxidative phosphorylation subunits and glycolysis enzymes are dysregulated in DS BFCNs.
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