ArticleCureus2023
SOX9 Expression Is Increased in Alzheimer's Disease (AD) and Is Associated With Disease Progression and APOE4 Genotype: A Computational Approach.
Article in Cureus, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Astrocytic Sox9 overexpression in Alzheimer's disease mouse models promotes Aβ plaque phagocytosis and preserves cognitive function.Nature neuroscience · 2026Article
- A Mouse Model of Sporadic Alzheimer's Disease with Elements of Major Depression.Molecular neurobiology · 2025Article
- Network Analysis of Brain and Bone Tissue Transcripts Reveals Shared Molecular Mechanisms Underlying Alzheimer's Disease and Related Dementias and Osteoporosis.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
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1 author at 1 institution in 1 country.
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Abstract
introductionAlzheimer's disease (AD) is a neurodegenerative disease characterized by depositions of amyloid-β protein leading to neuronal loss. Despite our understanding of the disease several gaps remain, including the role of astrocytes and astrocytic genes in the disease development and progression. Recently, some reports have suggested that SOX9 transcription factor (TF), an important mediator of astrocyte differentiation and maturation, might be linked to AD. Using human AD publicly available dataset, we aimed to analyze SOX9 expression and its relation to disease. METHODOLOGY: The AD gene expression data set was obtained from National Center for Bioinformatics-Gene Expression Omnibus (NCBI-GEO). The GSE48350 consisted of mRNA microarray data from 55 normal controls (173 samples) and 26 AD cases (81 samples) obtained, from four brain regions. The SOX9 expression profile and correlations were analyzed using the R2 Genomics Analysis and Visualization platform.
resultsThe SOX9 was significantly upregulated (p<0.001) in AD tissue compared to control cases. The increased expression appeared to be more in the entorhinal cortex (EC) and hippocampus (HC) regions. The SOX9 expression positively correlated with BRAAK stages (p<0.05). Interestingly in AD patients the SOX9 expression was significantly less in APOE3/3 genotypes compared with genotypes containing APOE4 allele. The SOX9 expression negatively correlated with oxidative phosphorylation genes which could suggest a metabolic role for the TF.
conclusionFrom these data we hypothesize that SOX9 acts as a metabolic regulator responding to lipid metabolism disruption associated with APOE4 genotypes. In turn, SOX9 expression could be associated with astrocyte maturation and survival in the disease contributing thus to disease burden and disease progression.
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