ArticleAJNR. American journal of neuroradiology2024
Imaging Transcriptomics of Brain Functional Alterations in MS and Neuromyelitis Optica Spectrum Disorder.
Article in AJNR. American journal of neuroradiology, 2024. 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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Who cites it
3 citing papers in PubMed.
- Temporal Dynamics of APOE and TREM2 Expression in Microglial Activation of NMOSD Mouse Models.Molecular neurobiology · 2025Article
- Spatiotemporal subtypes of brain and spinal cord atrophy in neuromyelitis optica spectrum disorders and multiple sclerosis.BMC medicine · 2025Article
- Lesion filling index predicts brain arteriovenous malformation obliteration after Gamma knife radiosurgery: a hemodynamic analysis.Neurosurgical review · 2024Article
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Authors and funding
16 authors.
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Abstract
background and purposeThe underlying transcriptomic signatures driving brain functional alterations in MS and neuromyelitis optica spectrum disorder (NMOSD) are still unclear. MATERIALS AND
methodsRegional fractional amplitude of low-frequency fluctuation (fALFF) values were obtained and compared among 209 patients with MS, 90 patients with antiaquaporin-4 antibody (AQP4)+ NMOSD, 49 with AQP4- NMOSD, and 228 healthy controls from a discovery cohort. We used partial least squares (PLS) regression to identify the gene transcriptomic signatures associated with disease-related fALFF alterations. The biologic process and cell type-specific signature of the identified PLS genes were explored by enrichment analysis. The correlation between PLS genes and clinical variables was explored. A prospective independent cohort was used to validate the brain fALFF alterations and the repeatability of identified genes.
resultsMS, AQP4+ NMOSD, and AQP4- NMOSD showed decreased fALFF in cognition-related regions and deep gray matter, while NMOSD (both AQP4+ and AQP4-) additionally demonstrated lower fALFF in the visual region. The overlapping PLS1- genes (indicating that the genes were overexpressed as regional fALFF decreased) were enriched in response to regulation of the immune response in all diseases, and the PLS1- genes were specifically enriched in the epigenetics profile in MS, membrane disruption and cell adhesion in AQP4+ NMOSD, and leukocyte activation in AQP4- NMOSD. For the cell type transcriptional signature, microglia and astrocytes accounted for the decreased fALFF. The fALFF-associated PLS1- genes directly correlated with Expanded Disability Status Scale of MS and disease duration across disorders.
conclusionsWe revealed the functional activity alterations and their underlying shared and specific gene transcriptional signatures in MS, AQP4+ NMOSD, and AQP4- NMOSD.
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