Yen-Feng Wang obtained his MD degree from National Yang-Ming University School of Medicine, Taiwan, and completed his neurology residency training in the Department of Neurology, Taipei Veterans General Hospital. He did his fellowship training in headache medicine with Professors Shuu-Jiun Wang and Jong-Ling Fuh, and earned his PhD degree from the Institute of Clinical Medicine, National Yang-Ming University. He is currently an attending physician and the Section Chief of the Division of General Neurology of the Department of Neurology, Taipei Veterans General Hospital, and also a professor of neurology of College of Medicine, National Yang Ming Chiao Tung University. His major research interests focus on the clinical and neuroimaging aspects of headache and pain disorders.
22 MARCH
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Session |
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11:00
12:30
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Diabetic Neuropathy: from Pathophysiology to Clinical Practice
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Chih-Cheng ChenTaiwan
Speaker
Pathophysiological Mechanisms Underlying Diabetic NeuropathyDiabetic neuropathy is a prevalent complication of both type I and type II diabetes mellitus. However, although peripheral nerve degeneration is highly associated with painful neuropathy, the underlying mechanism remains largely unknown. Here we report a role of advillin in painful diabetic neuropathy in a mouse model of type I diabetes induced by multiple low doses of streptozotocin (STZ). Advillin is an actin-binding protein involved in regulating the organization of actin filaments and the dynamics of axonal growth cones. In mice, advillin is exclusively expressed in somatosensory neurons, ubiquitously expressed in all neuron subtypes during neonatal ages and particularly enriched in isolectin B4 positive (IB4+) non peptidergic neurons in adulthood. We previously showed that advillin plays a key role in axon regeneration of somatosensory neurons during peripheral neuropathy. Mice lacking advillin lost the ability to recover form neuropathic pain induced by oxaliplatin, chronic compression of sciatic nerve, and experimental autoimmune encephalitis. In the diabetic model, STZ-induced cold allodynia was resolved in 8 weeks in wild type (Avil+/+) mice, but could last more than 30 weeks in advillin-knockout (Avil-/-) mice. Additionally, Avil-/- but not Avil+/+ mice showed STZ-induced mechanical hypersensitivity of muscle. Consistent with the prolonged and/or worsened STZ-induced neuropathic pain, second-line coping responses to pain stimuli were greater in Avil-/- than in Avil+/+ mice. On analyzing intraepidermal nerve density, STZ induced large axon degeneration in the hind paws but with distinct patterns between Avil+/+ and Avil-/- mice. We next probed whether advillin knockout could disturb capsaicin induced axon regeneration ex vivo because capsaicin is clinically used to treat painful diabetic neuropathy by promoting axon regeneration. In a primary culture of dorsal root ganglion cells, 10 min capsaicin treatment selectively promoted neurite outgrowth of IB4+ neurons in Avil+/+ but not Avil-/- groups, which suggests that capsaicin could reprogram the intrinsic axonal regeneration by modulating the advillin-mediated actin dynamics. Together, advllin-dependent IB4+ axon regeneration plays an important role in the development of painful diabetic neuropathy.
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Chi-Chao ChaoTaiwan
Speaker
Clinical Presentation and Diagnostic Evaluation of Diabetic Neuropathy
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Yen-Feng Wang Taiwan
Speaker
Evidence-Based Management of Diabetic Neuropathy: Pharmacologic and Non-Pharmacologic Approaches
102
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