TY - JOUR
T1 - Multi-omics profiling in spinal muscular atrophy (SMA)
T2 - investigating lipid and metabolic alterations through longitudinal CSF analysis of Nusinersen-treated patients
AU - Zandl-Lang, Martina
AU - Züllig, Thomas
AU - Holzer, Michael
AU - Eichmann, Thomas O
AU - Darnhofer, Barbara
AU - Schwerin-Nagel, Annette
AU - Zobel, Joachim
AU - Haidl, Harald
AU - Biebl, Ariane
AU - Köfeler, Harald
AU - Plecko, Barbara
N1 - © 2025. The Author(s).
PY - 2025/2/4
Y1 - 2025/2/4
N2 - Spinal muscular atrophy (SMA) is a rare neuromuscular disease caused by biallelic mutations in the SMN1 gene, leading to progressive muscle weakness due to degeneration of the anterior horn cells. Since 2017, SMA patients can be treated with the anti-sense oligonucleotide Nusinersen, which promotes alternative splicing of the SMN2 gene, by regular intrathecal injections. In this prospective study, we applied metabolomic, lipidomic, and proteomic analysis to examine sequential CSF samples from 13 SMA patients and controls. This multi-omic approach identified over 800 proteins and 400 small molecules including lipids. Multivariate analysis of multi-omic data successfully discriminated between the CSF derived from SMA patients and control subjects. Lipidomic analysis revealed increased levels of cholesteryl esters and lyso-phospholipids, along with reduced levels of cholesterol and phospholipids in the CSF of SMA patients as compared to healthy controls. These data, combined with results from functional assays, led us to conclude that SMA patients exhibit altered levels and function of high-density-lipoprotein (HDL)-like particles in the CSF. Notably, Nusinersen therapy was observed to reverse disease-specific profile changes toward a physiological state, potentially explicable by restoring HDL function.
AB - Spinal muscular atrophy (SMA) is a rare neuromuscular disease caused by biallelic mutations in the SMN1 gene, leading to progressive muscle weakness due to degeneration of the anterior horn cells. Since 2017, SMA patients can be treated with the anti-sense oligonucleotide Nusinersen, which promotes alternative splicing of the SMN2 gene, by regular intrathecal injections. In this prospective study, we applied metabolomic, lipidomic, and proteomic analysis to examine sequential CSF samples from 13 SMA patients and controls. This multi-omic approach identified over 800 proteins and 400 small molecules including lipids. Multivariate analysis of multi-omic data successfully discriminated between the CSF derived from SMA patients and control subjects. Lipidomic analysis revealed increased levels of cholesteryl esters and lyso-phospholipids, along with reduced levels of cholesterol and phospholipids in the CSF of SMA patients as compared to healthy controls. These data, combined with results from functional assays, led us to conclude that SMA patients exhibit altered levels and function of high-density-lipoprotein (HDL)-like particles in the CSF. Notably, Nusinersen therapy was observed to reverse disease-specific profile changes toward a physiological state, potentially explicable by restoring HDL function.
KW - Humans
KW - Oligonucleotides/therapeutic use
KW - Male
KW - Female
KW - Muscular Atrophy, Spinal/cerebrospinal fluid
KW - Child
KW - Child, Preschool
KW - Longitudinal Studies
KW - Metabolomics
KW - Proteomics
KW - Adolescent
KW - Prospective Studies
KW - Adult
KW - Lipidomics
KW - Lipid Metabolism/drug effects
KW - Young Adult
KW - Multiomics
UR - https://www.scopus.com/pages/publications/85218052415
U2 - 10.1007/s00415-025-12909-4
DO - 10.1007/s00415-025-12909-4
M3 - Article
C2 - 39904776
SN - 1432-1459
VL - 272
SP - 183
JO - Journal of Neurology
JF - Journal of Neurology
IS - 3
M1 - 183
ER -