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Condition: Peripheral Neuropathy

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Total 41 results found since Jan 2013.

Safety of antisense oligonucleotide and siRNA-based therapeutics.
The objectives were to assess factors that could contribute to the specific toxicities observed with these two classes of promising drug, and get a better understanding of the potential mechanism(s) responsible for these rare, but serious, adverse events. PMID: 28159625 [PubMed - as supplied by publisher]
Source: Drug Discovery Today - January 30, 2017 Category: Drugs & Pharmacology Authors: Chi X, Gatti P, Papoian T Tags: Drug Discov Today Source Type: research

Pmp22 mutant allele-specific siRNA alleviates demyelinating neuropathic phenotype in vivo.
In this study, we investigated whether regulation of a mutant allele by an allele-specific small interfering RNA (siRNA) can alleviate the demyelinating neuropathic phenotype of CMT. We designed 19 different allele-specific siRNAs for Trembler J (Tr-J) mice harboring a naturally occurring mutation (Leu16Pro) in Pmp22. Using a luciferase assay, we identified an siRNA that specifically and selectively reduced the expression level of the mutant allele and reversed the low viability of Schwann cells caused by mutant Pmp22 over-expression in vitro. The in vivo efficacy of the allele-specific siRNA was assessed by its intraperit...
Source: Neurobiology of Disease - January 16, 2017 Category: Neurology Authors: Lee JS, Chang EH, Koo OJ, Jwa DH, Mo WM, Kwak G, Moon HW, Park HT, Hong YB, Choi BO Tags: Neurobiol Dis Source Type: research

Overexpression of Protocadherin-10 in Transthyretin-Related Familial Amyloidotic Polyneuropathy.
Abstract Overwhelming data suggest that oncogenic and neurodegenerative pathways share several altered cellular responses to insults such as oxidative stress, extracellular matrix remodeling, inflammation, or cell dyscommunication. Protocadherin-10 (Pcdh10) is an adhesion molecule found to protect against tumorigenesis and essential for axonal elongation and actin dynamics during development. Here, by using genome microarrays we identified for the first time Pcdh10 up-regulation in tissues from transgenic mouse models, cultured Schwann cells, and human samples from a familial form of peripheral neuropathy (familia...
Source: The American Journal of Pathology - June 25, 2016 Category: Pathology Authors: Gonçalves NP, Martins D, Saraiva MJ Tags: Am J Pathol Source Type: research

Neuropathy Associated HSPB1 Mutations Result in Loss of Neuroprotection in an In Vitro Model of Astrocyte Toxicity to Motor Neurons (P5.021)
Conclusions:Expression of HSPB1 in astrocytes influences motor neuron viability. Our results suggest that the expression of HSPB1 mutations that are associated with an axonal hereditary neuropathy have the potential to exert deleterious effects on motor neurons in a non-cell autonomous manner.Disclosure: Dr. Heilman has nothing to disclose. Dr. Song has nothing to disclose. Dr. Miranda has nothing to disclose. Dr. Meyer has nothing to disclose. Dr. Best has nothing to disclose. Dr. Kaspar has nothing to disclose. Dr. Kolb has nothing to disclose.
Source: Neurology - April 3, 2016 Category: Neurology Authors: Heilman, P., Song, S., Miranda, C., Meyer, K., Best, C., Kaspar, B., Kolb, S. Tags: Genetics of Peripheral Neuropathies Source Type: research

Upregulation of CCL2 via ATF3/c-Jun interaction mediated the Bortezomib-induced peripheral neuropathy
Publication date: Available online 10 November 2015 Source:Brain, Behavior, and Immunity Author(s): Cuicui Liu, Shuo Luan, Handong OuYang, Zhenzhen Huang, Shaoling Wu, Chao Ma, Jiayou Wei, Wenjun Xin Bortezomib (BTZ) is a frequently used chemotherapeutic drug for the treatment of refractory multiple myeloma and hematological neoplasms. The mechanism by which the administration of BTZ leads to painful peripheral neuropathy remains unclear. In present study, we found that application of BTZ at 0.4 mg/kg for consecutive 5 days significantly increased the expression of CCL2 in DRG, and intrathecal administration of n...
Source: Brain, Behavior, and Immunity - November 13, 2015 Category: Neurology Source Type: research

Upregulation of CCL2 via ATF3/c-Jun interaction mediated the Bortezomib-induced peripheral neuropathy.
Abstract Bortezomib (BTZ) is a frequently used chemotherapeutic drug for the treatment of refractory multiple myeloma and hematological neoplasms. The mechanism by which the administration of BTZ leads to painful peripheral neuropathy remains unclear. In present study, we found that application of BTZ at 0.4 mg/kg for consecutive 5 days significantly increased the expression of CCL2 in DRG, and intrathecal administration of neutralizing antibody against CCL2 inhibited the mechanical allodynia induced by BTZ. We also found an increased expression of c-Jun in DRG, and that inhibition of c-Jun signaling prevented the...
Source: Brain, Behavior, and Immunity - November 7, 2015 Category: Neurology Authors: Liu C, Luan S, OuYang H, Huang Z, Wu S, Ma C, Wei J, Xin W Tags: Brain Behav Immun Source Type: research

HMGB-1 as a Potential Target for the Treatment of Diabetic Retinopathy.
CONCLUSIONS As a therapeutic target, HMGB-1 can inhibit inflammation and promote RGCs survival to delay DR progress through the HMGB-1-TLR4-NF-κB signaling pathway. PMID: 26454330 [PubMed - as supplied by publisher]
Source: Medical Science Monitor - October 14, 2015 Category: Research Tags: Med Sci Monit Source Type: research

Synergistic anti‐myeloma activity of the proteasome inhibitor marizomib and the IMiD® immunomodulatory drug pomalidomide
Abstract The proteasome inhibitor bortezomib is an effective therapy for the treatment of relapsed and refractory multiple myeloma (RRMM); however, prolonged treatment can be associated with toxicity, peripheral neuropathy and drug resistance. Our earlier studies showed that the novel proteasome inhibitor marizomib is distinct from bortezomib in its chemical structure, mechanisms of action and effects on proteasomal activities, and that it can overcome bortezomib resistance. Pomalidomide, like lenalidomide, has potent immunomodulatory activity and has been approved by the US Food and Drug Administration for the treatment o...
Source: British Journal of Haematology - October 12, 2015 Category: Hematology Authors: Deepika S. Das, Arghya Ray, Yan Song, Paul Richardson, Mohit Trikha, Dharminder Chauhan, Kenneth C. Anderson Tags: Research Paper Source Type: research

APE1, the DNA base excision repair protein, regulates the removal of platinum adducts in sensory neuronal cultures by NER
Publication date: Available online 26 June 2015 Source:Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis Author(s): Hyun-Suk Kim , Chunlu Guo , Eric L. Thompson , Yanlin Jiang , Mark R. Kelley , Michael R. Vasko , Suk-Hee Lee 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...
Source: Mutation Research Fundamental and Molecular Mechanisms of Mutagenesis - June 26, 2015 Category: Cytology Source Type: research

Abstract 3489: A novel investigation into chemotherapy-induced peripheral neuropathy using iPSC-derived human neurons
Chemotherapy-induced peripheral neuropathy (CIPN) is the major dose-limiting side effect of many anti-cancer drugs including taxanes, vinca alkaloids and platinating agents. These drugs represent standard of care for common cancers, however there are no effective treatments and no means to identify patients at risk for CIPN. The mechanisms underlying CIPN have not been precisely determined and few human neuronal models to study CIPN exist. Recent technology has allowed for the differentiation of induced pluripotent stem cells (iPSC) to human neurons. We have utilized genetically diverse human neurons as a model to study th...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Komatsu, M., Wheeler, H. E., Wing, C., Delaney, S., Dolan, M. E. Tags: Molecular and Cellular Biology Source Type: research

Integration of cell line and clinical trial genome-wide analyses supports a polygenic architecture of paclitaxel-induced sensory peripheral neuropathy.
CONCLUSIONS: The enrichment results and functional example imply that cellular models of chemotherapeutic toxicity may capture components of the underlying polygenic architecture of related traits in patients. PMID: 23204130 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - November 30, 2012 Category: Cancer & Oncology Authors: Wheeler HE, Gamazon ER, Wing C, Njiaju UO, Njoku C, Baldwin RM, Owzar K, Jiang C, Watson D, Shterev I, Kubo M, Zembutsu H, Winer EP, Hudis CA, Shulman L, Nakamura Y, Ratain MJ, Kroetz D, Cox NJ, Dolan ME Tags: Clin Cancer Res Source Type: research