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Transcriptomic imputation identifies tissue-specific genes associated with cervical myelopathy.

Carina Seah1, Mert Karabacak2, Konstantinos Margetis2

  • 1Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Neurosurgery, Mount Sinai Health System, New York, NY, USA.

The Spine Journal : Official Journal of the North American Spine Society
|November 4, 2024
PubMed
Summary

Genetic predisposition to degenerative cervical myelopathy (DCM) involves tissue-specific gene expression. Candidate drugs identified may reverse these genetic signatures, offering new therapeutic avenues for DCM patients.

Keywords:
BiobankCervical myelopathyGenetic riskTranscriptomic imputation

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Area of Science:

  • Genetics
  • Neurology
  • Pharmacology

Background:

  • Degenerative cervical myelopathy (DCM) is a progressive spinal condition causing neurological dysfunction.
  • Family history suggests a genetic component in DCM incidence and progression.

Purpose of the Study:

  • To identify the tissue-specific, functional genetic basis of hereditary predisposition to cervical myelopathy.
  • To explore potential therapeutic interventions for DCM based on genetic findings.

Main Methods:

  • Retrospective case-control study utilizing patient genetics and electronic health records from a large urban biobank.
  • Transcriptomic imputation was applied to identify genetically regulated gene expression signatures associated with DCM.
  • Drug repurposing analysis was performed using the CMAP database to find compounds targeting DCM-associated gene signatures.

Main Results:

  • Sixteen genes were significantly associated with DCM across five tissues, indicating tissue-specific genetic risk.
  • Upregulated genes include HES6, PI16, TMEM183A, BDH2, LINC00937, CLEC4D, USP43, SPATA1.
  • Downregulated genes include TTC12, CDK5, PAFAH1B2, RCSD1, KLHL29, PTPRG, RP11-620J15.3, C1RL.
  • Twenty-two compounds were identified as potential therapeutics to reverse the DCM genetic signature.

Conclusions:

  • Inherited genetic risk for DCM is linked to genes in tissue-specific nociceptive and proliferative pathways.
  • Candidate therapeutics targeting nociceptive, calcium channel modulating, and antiproliferative effects may reverse these genetic signatures.
  • Understanding DCM's genetic basis enables personalized therapies and identifies novel drug candidates to improve patient outcomes.