Journal of the peripheral nervous system : JPNS
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Alterations in peripheral nervous system (PNS) insulin support may contribute to diabetic neuropathy (DN); yet, PNS insulin signaling is not fully defined. Here, we investigated in vivo insulin signaling in the PNS and compared the insulin responsiveness to that of muscle, liver, and adipose. Non-diabetic mice were administered increasing doses of insulin to define a dose-response relationship between insulin and Akt activation in the dorsal root ganglion (DRG) and sciatic nerve. ⋯ At a therapeutically relevant dose, Akt was activated in the muscle, liver, and adipose at 30 min, correlating with the changes in blood glucose levels. Interestingly, the sciatic nerve showed a similar signaling profile as insulin-sensitive tissues; however, there was not a comparable activation in the DRG or spinal cord. These results present new evidence regarding PNS insulin signaling pathways in vivo and provide a baseline for studies investigating the contribution of disrupted PNS insulin signaling to DN pathogenesis.
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Understanding of Guillain-Barré syndrome (GBS) has progressed substantially since the seminal 1916 report by Guillain et al. Although Guillain, Barré, and Strohl summarised the syndrome based on observations of two French infantrymen, 2012 saw the beginning of an ambitious collaborative study designed to collect detailed data from at least 1,000 patients worldwide (IGOS, www.gbsstudies.org/about-igos). Progress has been made in many areas even since GBS was last reviewed in this journal in 2009. ⋯ In other areas, management has improved. Antibiotic prophylaxis in ventilated patients reduces respiratory tract infection, thromboprophylaxis has reduced the risk of venous thromboembolism, and there is increasing awareness of the benefit of high-intensity rehabilitation. This article highlights some of the interesting and thought-provoking developments of the last 3 years, and is based on a plenary lecture given at the 2012 Peripheral Nerve Society (PNS) meeting.
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J. Peripher. Nerv. Syst. · Mar 2013
Challenges in developing novel therapies for peripheral neuropathies: a summary of The Foundation for Peripheral Neuropathy Scientific Symposium 2012.
On March 14-16, 2012, The Foundation for Peripheral Neuropathy organized a scientific meeting that brought together basic and clinical scientists studying peripheral neuropathies and mechanisms of axonal degeneration and representatives from the drug industry, National Institutes of Health, and Federal Drug Administration. This meeting summary covers the main discussion points laid out by the participants that hamper development of novel therapies for peripheral neuropathies and neuropathic pain. In each section of the meeting, the discussion was led by a keynote talk and was followed by a panel of discussants that were asked to bring two key questions in their areas of research. With audience participation, this format led to a lively discussion that pointed out the deficiencies in both animal modeling of human diseases and issues in clinical trial design unique to the peripheral neuropathies and neuropathic pain.
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J. Peripher. Nerv. Syst. · Dec 2012
Case Reports Historical ArticleHereditary neuropathy with liability to pressure palsies. Diagnosis in the first family (1947) confirmed.
In 1947, the Dutch neurologist De Jong published the first family with, what later would be called, hereditary neuropathy with liability to pressure palsies (HNPP). We recently found a new case from this family and were able to confirm the diagnosis by DNA analysis.
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J. Peripher. Nerv. Syst. · Sep 2012
PARP inhibitors attenuate chemotherapy-induced painful neuropathy.
Chemotherapy-induced peripheral neuropathy (CIPN) is a major toxicity of chemotherapy treatment for which no therapy is approved. Poly(ADP-ribose) polymerase (PARP)1/2 are nuclear enzymes activated upon DNA damage, and PARP1/2 inhibition provides resistance against DNA damage. A role for PARP inhibition in sensory neurotransmission has also been established. ⋯ Mechanical allodynia was observed in rats treated with vincristine. PARP1/2 inhibition significantly attenuated development of mechanical allodynia and reduced poly ADP-ribose (PAR) activation in rat skin. The data presented here show that PARP inhibition attenuates vincristine-induced mechanical allodynia in rats, and supports that PARP inhibition may represent a novel therapeutic approach for CIPN.