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Transcriptomic Analysis and Multiple Machine Learning Approaches Identify ZDHHC20 and Its Highly Correlated Gene AK5
Zhipeng Lu1, Zhongqi Li2, Zhibiao Yin1
1Department of Neurology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Journal of Molecular Neuroscience : MN
|May 16, 2026
Summary
Multiple system atrophy (MSA), a fatal neurodegenerative disease, shows reduced levels of ZDHHC20 and AK5 genes, particularly in oligodendrocytes. These genes are linked to mitochondrial dysfunction and may serve as novel biomarkers for MSA diagnosis.
Area of Science:
- Neuroscience
- Genetics
- Biochemistry
Background:
- Multiple system atrophy (MSA) is a fatal neurodegenerative disorder with limited diagnostic methods.
- The role of protein palmitoylation in MSA pathogenesis is currently unknown.
- Effective biomarkers for early MSA diagnosis are urgently needed.
Purpose of the Study:
- To investigate the role of protein palmitoylation in MSA pathogenesis.
- To identify potential diagnostic biomarkers for MSA.
- To explore the molecular mechanisms underlying MSA.
Main Methods:
- Integrated bulk and single-nucleus RNA sequencing (snRNA-seq) from postmortem MSA brain tissues.
- Employed eight machine learning algorithms to screen palmitoylation-related genes.
- Conducted functional enrichment, cellular deconvolution, and pseudotime trajectory analyses.
Main Results:
- Identified ZDHHC20 and its correlated gene AK5 as key hub genes.
- Observed significant downregulation of ZDHHC20 and AK5 in MSA brain tissues, especially in cerebellar white matter.
- Linked ZDHHC20 and AK5 downregulation to mitochondrial dysfunction and impaired energy metabolism.
- snRNA-seq revealed predominant expression in oligodendrocytes with reduced developmental trajectory expression in MSA.
Conclusions:
- ZDHHC20 and AK5 are promising novel biomarkers for Multiple System Atrophy (MSA).
- These findings offer new insights into MSA diagnosis and potential therapeutic targets.
- The study highlights the involvement of protein palmitoylation in MSA pathogenesis.
