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A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
Published on: October 20, 2016
Neurovascular-Immune Biomarkers in Ménière Disease: Insights From High-Throughput Proteomics
Giuseppe Chiarella1, Giovanni Cuda2, Elvira I Parrotta3
1Department of Experimental and Clinical Medicine, Unit of Audiology, Phoniatrics and Vestibology, Regional Centre for Cochlear Implants and ENT Diseases, University "Magna Graecia", Catanzaro, Italy.
Background:
Ménière disease (MD) is a chronic inner ear disorder characterized by recurrent vertigo, fluctuating sensorineural hearing loss, tinnitus, and aural fullness. Diagnosis is clinical, and no validated peripheral biomarkers are available. Although endolymphatic hydrops is a hallmark, its poor correlation with symptom severity suggests broader systemic mechanisms.
Methods:
We performed large-scale serum proteomic profiling using the Olink Explore HT platform, quantifying 5400 proteins in patients with definite MD and matched controls. After quality control, 1037 proteins were analyzed through differential expression, protein-protein interaction mapping, and systems biology approaches.
Results:
MD exhibited a structured systemic proteomic signature characterized by 3 functionally integrated protein families in the upregulated proteome: (1) neuroendocrine and fluid-regulatory mediators (NPPB, POMC, CCK, NPY) converging on pathways controlling fluid homeostasis and HPA axis signaling; (2) morphogenetic and tissue-remodeling proteins (BMP6, SOST, FRZB, RSPO/SFRP) supporting extracellular matrix plasticity; and (3) cellular stress-adaptation proteins (FARSA, WARS1, BAG3) involved in translational control and proteostasis. The downregulated proteome revealed coordinated suppression of epithelial maintenance factors (EGF, SBDS) and neutrophil immune effectors (MMP8, OLFM4, RNASE3) alongside attenuation of NF-κB signaling, indicating dysregulation of tissue repair and immune surveillance rather than hyperinflammation. Tissue enrichment highlighted autonomic and vascular compartments in the upregulated signature, while neutrophil and hematopoietic lineages dominated the downregulated profile, supporting a neurovascular-immune interface.
Conclusions:
MD emerges as a systemic neurovascular-immune disorder characterized by activation of compensatory neuroendocrine-vascular-proteostatic pathways coupled with dysregulation of tissue repair and immune effector mechanisms, rather than solely a hydropic condition. The identified serum proteomic signature provides a candidate biomarker framework for diagnostic support, patient stratification, and future longitudinal validation.
Insights
Ménière disease (MD) is a systemic neurovascular-immune disorder, not just an inner ear issue. Proteomic analysis reveals key biomarkers for diagnosis and patient stratification.
Area of Science:
- Biochemistry
- Immunology
- Genomics
Background:
- Ménière disease (MD) is a chronic inner ear disorder with symptoms including vertigo, hearing loss, tinnitus, and aural fullness.
- Current diagnosis is clinical, lacking validated peripheral biomarkers.
- While endolymphatic hydrops is a known factor, its correlation with symptom severity is weak, suggesting broader systemic involvement.
Purpose of the Study:
- To investigate the systemic proteomic signature of Ménière disease (MD).
- To identify potential peripheral biomarkers for MD diagnosis and patient stratification.
Main Methods:
- Large-scale serum proteomic profiling of 5400 proteins using the Olink Explore HT platform.
- Analysis of 1037 proteins in patients with definite MD and matched controls.
- Application of differential expression, protein-protein interaction mapping, and systems biology approaches.
Main Results:
- MD shows a distinct proteomic signature with upregulated neuroendocrine, fluid-regulatory, morphogenetic, tissue-remodeling, and cellular stress-adaptation proteins.
- Downregulated proteins include epithelial maintenance factors and neutrophil immune effectors, indicating impaired tissue repair and immune surveillance rather than hyperinflammation.
- Tissue enrichment analysis points to autonomic, vascular, neutrophil, and hematopoietic compartments, suggesting a neurovascular-immune interface.
Conclusions:
- Ménière disease (MD) is characterized as a systemic neurovascular-immune disorder with activated compensatory pathways and dysregulated tissue repair/immune mechanisms.
- The identified serum proteomic signature offers a framework for diagnostic biomarkers, patient stratification, and future research.
