We are excited to announce our latest publication in the Journal of Translational Medicine, where we investigate inflammatory and complement-related biomarkers in the aqueous humour of patients with non-exudative age-related macular degeneration (AMD). Our study aims to enhance our understanding of disease mechanisms and identify potential diagnostic markers.
Why study the aqueous humour in AMD?
AMD is a leading cause of vision loss in the elderly, with disease progression driven by chronic inflammation and dysregulation of the complement system. While blood-based biomarkers have previously been investigated, studying the aqueous humour (the fluid in the anterior chamber of the eye) provides a more direct approach to local inflammatory processes within the retina.
Key findings
In this study, we analysed 78 inflammatory and complement proteins in aqueous humour samples from non-exudative AMD patients and controls. Our results highlight several important findings:
Complement proteins in aqueous humour: We detected high levels of complement components, including iC3b, FH/FHL-1, C4B, and FI.
Reduced C4 and IL-10 levels in AMD: Patients with non-exudative AMD showed significantly decreased levels of complement component C4 and the anti-inflammatory cytokine IL-10, suggesting a potential role in disease progression. A non-significant trend towards reduced FI levels in AMD patients indicates a potential impairment in complement regulation.
Drusen volume correlations: Higher drusen volume, a hallmark of AMD, was positively correlated with CCL4 levels, suggesting a link between inflammation and disease severity.
Links to smoking and ageing: Smoking was associated with increased levels of pro-inflammatory proteins (CCL7, IL-7), and MMP-1 levels correlated with age, reinforcing known risk factors of AMD.
Sex-related variations in complement proteins: C4B and the complement regulators FB, FH/FHL-1, and FI exhibited decreased levels in females compared with those in males.
What does this mean?
These findings support the role of complement dysregulation and inflammation in AMD and highlight potential biomarkers for further investigation. As a pilot study, our work provides an initial overview, and we are now conducting a larger follow-up study with stratified cohorts to further validate these biomarkers.
We are excited about the potential impact of these findings on AMD research and early disease detection. We look forward to sharing more insights as we continue investigating the molecular mechanisms driving retinal degeneration.
Read the full paper here: 10.1186/s12967-024-05909-x
Juliane
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