New biomarkers of inflammation identified as risk of polyneuropathy

Polyneuropathy is one of the most common complications in individuals with diabetes. However, it can likewise happen with certain risk factors or diseases before the beginning of diabetes. First symptoms are frequently pins-and-needles sensations in the feet. Although polyneuropathy is present in about 30% of people with diabetes, it frequently remains undiagnosed. Researchers have now been able to show for the first time that six biomarkers of inflammation show the risk of polyneuropathy.   

Although many patients suffer from polyneuropathy, relatively little is currently known about its development, which additionally limits the therapeutic options. It is known that inflammatory processes add to other diabetic complications such as stroke or heart attack. The aim of this new examination was therefore the extensive analysis of biomarkers that describe inflammatory processes as a risk factor for distal sensory polyneuropathy (DSPN).  The two individuals with type 2 diabetes and people in the elderly general population were analysed.

In their study, they identified novel biomarkers that show the risk of polyneuropathy. For the first time, researchers were also able to find indications that in addition to the innate immune system, the adaptive immune system could be involved in the development of the disease. These findings could open new therapeutic perspectives. The aim could be to impact the immune system accordingly and thus ultimately prevent the development or progression of neuropathy.

Study -- Procedure and Design

The examination included 513 men and women of the population-based KORA F4/FF4 cohort aged 62 to 81 years who had no distal sensory polyneuropathy at the beginning of the study. Of these people, 127 developed a distal sensory polyneuropathy during the 6.5 year follow-up period. The serum level of 26 of these 71 biomarkers was higher in individuals who developed polyneuropathy during the study than in people without polyneuropathy. After statistical correction for multiple testing, higher concentrations of six biomarkers remained related with the distal sensory polyneuropathy risk.   

The chemokines indicates neurotoxic effects in a cell culture model, which showed their involvement in the development of neuropathy. When the data for these six biomarkers were added to a clinical risk model, the predictive quality of the model enhanced significantly. Further pathway examinations showed that different cell types of innate and adaptive immunity are likely to be involved in the development of DSPN. Overall, this examination has therefore been able to reveal novel relationship between biomarkers of inflammation and the risk of polyneuropathy and to give evidence suggesting a complex interaction of adaptive and innate immunity in the development of this complication.  

Conclusion

This examination significantly improves understanding of the role of inflammatory processes in the improvement of DSPN in the elderly both with and without type 2 diabetes. The primary findings must now be replicated in other cohorts. In addition to biochemical examinations, examinations of immune cells are also important. The long-term aim of this work is to clarify whether and how modulation of inflammatory processes can supplement the options for prevention and therapy of DSPN.

Contact details:
Tiffany Hales
Program Manager | Diabetic 2018
Email id: diabetes@mehealthevents.org