Inflammation and Neurodegeneration in Glaucoma: Isolated Eye Disease or a Part of a Systemic Disorder? - Serum Proteomic Analysis.

Introduction: Glaucoma is the most common optic neuropathy and the leading cause of irreversible blindness worldwide, which affects 3.54% of the population aged 40-80 years. Despite numerous published studies, some aspects of glaucoma pathogenesis, serum biomarkers, and their potential link with other diseases remain unclear. Recent articles have proposed that autoimmune, oxidative stress and inflammation may be involved in the pathogenesis of glaucoma. Methods: We investigated the serum expression of 92 inflammatory and neurotrophic factors in glaucoma patients. The study group consisted of 26 glaucoma patients and 192 healthy subjects based on digital fundography. Results: Patients with glaucoma had significantly lower serum expression of IL-2Rß, TWEAK, CX3CL1, CD6, CD5, LAP TGF-beta1, LIF-R, TRAIL, NT-3, and CCL23 and significantly higher expression of IL-22Rα1. Conclusion: Our results indicate that patients with glaucoma tend to have lower levels of neuroprotective proteins and higher levels of neuroinflammatory proteins, similar to those observed in psychiatric, neurodegenerative and autoimmune diseases, indicating a potential link between these conditions and glaucoma pathogenesis.

The prevalence of age-related macular degeneration and osteoporosis in the older Polish population: Is there a link?

BACKGROUND: Age-related macular degeneration is the primary cause of irreversible blindness in developed countries, whereas the global prevalence of osteoporosis-a major public health problem-is 19.7%. Both diseases may coincide in populations aged >50 years, leading to serious health deterioration and decreased quality of life. OBJECTIVES: This study aimed to analyze the relationship between age-related macular degeneration and osteopenia, defined as decreased bone mineral density, in the Polish population. METHODS: Participants were derived from the population-based Bialystok PLUS Study. Randomized individuals were stratified into two groups, those with age-related macular degeneration (AMD-1 group) or without age-related macular degeneration (AMD-0 group). Using a cutoff value of -1.0 to identify low bone mass, participants with femoral bone mineral density T-scores above -1.0 were assigned to the normal reference, and those with T-scores below -1.0 were assigned to the osteopenia category. Among 436 Caucasian participants aged 50-80 years (252 women, 184 men), the prevalence of age-related macular degeneration was 9.9% in women and 12.0% in men. Decreased bone mineral density based on T-scores was observed in 36.9% of women and in 18.9% of men. Significant differences in femoral bone mineral density between the AMD-0 and AMD-1 groups were detected only in men (mean difference [95% confidence interval] = 0.11 (0.02; 0.13); p = 0.012 for femoral bone mineral density, and 0.73 [0.015; 0.94]; p = 0.011 for the femoral T-score). No associations were observed between bone mineral density and age-related macular degeneration in women. CONCLUSION: Decreased femoral bone mineral density may be associated with a higher risk of age-related macular degeneration in men, but a causal link remains unclear.

Elevated Plasma Levels of C1qTNF1 Protein in Patients with Age-Related Macular Degeneration and Glucose Disturbances.

In recent years, research has provided increasing evidence for the importance of inflammatory etiology in age-related macular degeneration (AMD) pathogenesis. This study assessed the profile of inflammatory cytokines in the serum of patients with AMD and coexisting glucose disturbances (GD). This prospective population-based cohort study addressed the determinants and occurrence of cardiovascular, neurological, ophthalmic, psychiatric, and endocrine diseases in residents of Bialystok, Poland. To make the group homogenous in terms of inflammatory markers, we analyzed only subjects with glucose disturbances (GD: diabetes or prediabetes). Four hundred fifty-six patients aged 50-80 were included. In the group of patients without macular degenerative changes, those with GD accounted for 71.7%, while among those with AMD, GD accounted for 89.45%. Increased serum levels of proinflammatory cytokines were observed in both AMD and GD groups. C1qTNF1 concentration was statistically significantly higher in the group of patients with AMD, with comparable levels of concentrations of other proinflammatory cytokines. C1qTNF1 may act as a key mediator in the integration of lipid metabolism and inflammatory responses in macrophages. Moreover, C1qTNF1 levels are increased after exposure to oxidized low-density lipoprotein (oxLDL), which plays a key role in atherosclerotic plaque formation and is also a major component of the drusen observed in AMD. C1qTNF1 may, therefore, prove to be a link between the accumulation of oxLDL and the induction of local inflammation in the development of AMD with concomitant GD.