AI Article Synopsis
- - This study examines lesioned fascicles in the sciatic nerves of people with diabetic neuropathy (DN) to understand how these lesions relate to clinical symptoms and their underlying mechanisms.
- - Using advanced imaging and proteomic analysis, researchers found that only individuals with type 2 diabetes (T2D) had these lesions, which showed significant damage like axonal degeneration and demyelination, along with a compromised blood nerve barrier (BNB).
- - The results indicate that while non-lesioned fascicles from T2D donors showed neuroprotective responses, lesioned ones did not and had increased inflammatory activity, suggesting a harmful connection between the liver and nerves that could be targeted for therapy.
Article Abstract
Lesioned fascicles (LFs) in the sciatic nerves of individuals with diabetic neuropathy (DN) correlate with clinical symptom severity. This study aimed to characterize the structural and molecular composition of these lesions to better understand DN pathogenesis. Sciatic nerves from amputees with and without type 2 diabetes (T2D) were examined using ex vivo magnetic resonance neurography, in vitro imaging, and proteomic analysis. Lesions were only found in T2D donors and exhibited significant structural abnormalities, including axonal degeneration, demyelination, and impaired blood-nerve barrier (BNB). Although non-LFs from T2D donors showed activation of neuroprotective pathways, LFs lacked this response and instead displayed increased complement activation via the classical pathway. The detection of liver-derived acute-phase proteins suggests that BNB disruption facilitates harmful interorgan communication between the liver and nerves. These findings reveal key molecular mechanisms contributing to DN and highlight potential targets for therapeutic intervention.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664024 | PMC |
| http://dx.doi.org/10.2337/db24-0493 | DOI Listing |
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