Toxic and drug-induced peripheral neuropathies

Diezi, Manuel; Buclin, Thierry; Küntzer, Thierry

doi:10.1097/wco.0b013e328364eb07

Cited by 23 publications

(21 citation statements)

References 94 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The majority of toxin-induced peripheral neuropathies are associated with axonopathies, as a result of insult to the axonal cytoskeleton or mitochondria (Diezi et al, 2013). The number of research publications concerning PNS gliotoxins is limited, although understanding the effects of local anesthetics on Schwann cells is of significance.…”

Section: Myelin Repair In Toxin-induced Neuropathiesmentioning

confidence: 99%

Promoting peripheral myelin repair

Zhou

Notterpek

2016

Experimental Neurology

View full text Add to dashboard Cite

Compared to the central nervous system (CNS), peripheral nerves have a remarkable ability to regenerate and remyelinate. This regenerative capacity to a large extent is dependent on and supported by Schwann cells, the myelin-forming glial cells of the peripheral nervous system (PNS). In a variety of paradigms, Schwann cells are critical in the removal of the degenerated tissue, which is followed by remyelination of newly-regenerated axons. This unique plasticity of Schwann cells has been the target of myelin repair strategies in acute injuries and chronic diseases, such as hereditary demyelinating neuropathies. In one approach, the endogenous regenerative capacity of Schwann cells is enhanced through interventions such as exercise, electrical stimulation or pharmacological means. Alternatively, Schwann cells derived from healthy nerves, or engineered from different tissue sources have been transplanted into the PNS to support remyelination. These transplant approaches can then be further enhanced by exercise and/or electrical stimulation, as well as by the inclusion of biomaterial engineered to support glial cell viability and neurite extension. Advances in our basic understanding of peripheral nerve biology, as well as biomaterial engineering, will further improve the functional repair of myelinated peripheral nerves.

show abstract

Section: Myelin Repair In Toxin-induced Neuropathiesmentioning

confidence: 99%

Promoting peripheral myelin repair

Zhou

Notterpek

2016

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…21 Other toxic exposures may disrupt metabolic homeostasis, myelin composition, and mitochondrial function, producing demyelinating and axonopathic disease to varying degrees. 22 …”

Section: Pathophysiologymentioning

confidence: 99%

The Importance of Rare Subtypes in Diagnosis and Treatment of Peripheral Neuropathy

et al. 2015

View full text Add to dashboard Cite

Importance-Peripheral neuropathy is a prevalent condition that usually warrants a thorough history and examination, but limited diagnostic evaluation. Rare localizations of peripheral neuropathy, however, often require more extensive diagnostic testing and different treatments.Objective-To describe rare localizations of peripheral neuropathy, including the appropriate diagnostic evaluation and available treatments.Evidence Review-References were identified from PubMed searches with an emphasis on systematic reviews and randomized clinical trials. Articles were also identified through the use of the author's own files. Search terms included common rare neuropathy localizations and their causes, as well as epidemiology, pathophysiology, diagnosis, and treatment.Findings-Diffuse, non-length dependent neuropathies, multiple mononeuropathies, polyradiculopathies, plexopathies, and radiculoplexus neuropathies are rare peripheral neuropathy localizations that often require extensive diagnostic testing. Atypical neuropathy features, such as acute/subacute onset, asymmetry, and/or motor predominant signs, are frequently present. The most common diffuse, non-length dependent neuropathies are Guillain-Barre syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy (MMN), and amyotrophic lateral sclerosis (ALS). Effective disease modifying therapies exist for many diffuse, non-length dependent neuropathies including GBS, CIDP, MMN, and some paraprotein-associated demyelinating neuropathies. Vasculitic neuropathy (multiple mononeuropathy) also has efficacious treatment options, but definitive evidence of a treatment effect for IgM anti-MAG neuropathy and diabetic amyoptrophy (radiculoplexus neuropathy) is lacking.Conclusions and Relevance-Recognition of rare localizations of periperhal neuropathy is essential given the implications for diagnostic testing and treatment. Electrodiagnostic studies are

show abstract

“…The severity of the neuropathy can warrant stopping therapy and in many cases, the toxicity is maintained after therapy is discontinued [8, 10, 11]. To date, there are no therapies available to prevent or reduce cisplatin-induced peripheral neuropathy (CIPN) although a number of agents have been tried [12]. …”

Section: Introductionmentioning

confidence: 99%

APE1, the DNA base excision repair protein, regulates the removal of platinum adducts in sensory neuronal cultures by NER

Kim

Guo

Thompson

et al. 2015

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

View full text Add to dashboard Cite

Peripheral neuropathy is one of the major side effects of treatment with the anticancer drug, cisplatin. One proposed mechanism for this neurotoxicity is the formation of platinum adducts in sensory neurons that could contribute to DNA damage. Although this damage is largely repaired by nuclear excision repair (NER), our previous findings suggest that augmenting the base excision repair pathway (BER) by overexpressing the repair protein APE1 protects sensory neurons from cisplatin-induced neurotoxicity. The question remains whether APE1 contributes to the ability of the NER pathway to repair platinum-damage in neuronal cells. To examine this, we manipulated APE1 expression in sensory neuronal cultures and measured Pt-removal after exposure to cisplatin. When neuronal cultures were treated with increasing concentrations of cisplatin for two or three hours, there was a concentration-dependent increase in Pt-damage that peaked at four hours and returned to near baseline levels after 24 hours. In cultures where APE1 expression was reduced by ~80% using siRNA directed at APE1, there was a significant inhibition of Pt-removal over eight hours which was reversed by overexpressing APE1 using a lentiviral construct for human wtAPE1. Reduction in APE1 expression also altered the expression of the NER proteins RPA70 and XPA in sensory neuronal cultures. Overexpressing a mutant APE1 (C65 APE1), which only has DNA repair activity, but not its other significant redox-signaling function, mimicked the effects of wtAPE1. Overexpressing DNA repair activity mutant APE1 (226+177APE1), with only redox activity was ineffective suggesting it is the DNA repair function of APE1 and not its redox-signaling, that restores the Pt-damage removal. Together, these data provide the first evidence that a critical BER enzyme, APE1, helps regulate the NER pathway in the repair of cisplatin damage in sensory neurons.

show abstract

Toxic and drug-induced peripheral neuropathies

Cited by 23 publications

References 94 publications

Promoting peripheral myelin repair

Promoting peripheral myelin repair

The Importance of Rare Subtypes in Diagnosis and Treatment of Peripheral Neuropathy

APE1, the DNA base excision repair protein, regulates the removal of platinum adducts in sensory neuronal cultures by NER

Contact Info

Product

Resources

About