{"id":{"repo_id":"ohiolink","oai_identifier":"oai:etd.ohiolink.edu:mco1365173843"},"canonical_url":"https://search.dev.ndltd.org/etd/ohiolink/oai:etd.ohiolink.edu:mco1365173843","repository":{"repo_id":"ohiolink","name":"OhioLINK","base_url":"https://etd.ohiolink.edu/acprod/odb_etd/ws/oai/oai"},"display":{"title":"The Role of Trophic Factors and Other Drugs in the Treatment of Huntington's Disease in R6/2 Mouse Model","abstract":"Huntington's disease (HD) is a rare, autosomal dominant, neurodegenerative disease, characterized by behavioral and cognitive deterioration, as well as a progressive loss in motor control. HD is thought to be caused by the expansion of trinucleotide, CAG, expansion at the N-terminus within exon 1 of the huntingtin gene. The huntingtin protein is considered to play a role in the cell survival and apoptosis pathways of neurons, including Akt kinase and JNK. We hypothesized that the treatment of the R6/2 transgenic mouse model with neurotrophic peptides, Colivelin and analogue dPEG-Colivelin, Sulforaphane, a compound that reduces oxidative stress, and Ceftriaxone, a GLT-1 upregulator, would attenuate motor behavioral abnormalities and neurodegeneration in HD R6/2 mouse model.Although we did not observe any behavioral motor improvement with Colivelin and dPEG-Colivelin, we did, in fact, find significant up-regulation of p-Akt in the ST of 40 mg/20g Colivelin treated R6/2 mice as compared to saline treated R6/2 mice. However, we did not observe any significant difference in the level of p-Akt in the PFC with Colivelin and dPEG-Colivelin treatments as compared to saline treated groups. Moreover, significant increase in p-JNK was observed in the ST and PFC of 40 mg/20g Colivelin treated R6/2 mice. Alternatively, we did not observe any behavioral improvements with Ceftriaxone or Sulforaphane.","abstract_html":"Huntington's disease (HD) is a rare, autosomal dominant, neurodegenerative disease, characterized by behavioral and cognitive deterioration, as well as a progressive loss in motor control. HD is thought to be caused by the expansion of trinucleotide, CAG, expansion at the N-terminus within exon 1 of the huntingtin gene. The huntingtin protein is considered to play a role in the cell survival and apoptosis pathways of neurons, including Akt kinase and JNK. We hypothesized that the treatment of the R6/2 transgenic mouse model with neurotrophic peptides, Colivelin and analogue dPEG-Colivelin, Sulforaphane, a compound that reduces oxidative stress, and Ceftriaxone, a GLT-1 upregulator, would attenuate motor behavioral abnormalities and neurodegeneration in HD R6/2 mouse model.Although we did not observe any behavioral motor improvement with Colivelin and dPEG-Colivelin, we did, in fact, find significant up-regulation of p-Akt in the ST of 40 mg/20g Colivelin treated R6/2 mice as compared to saline treated R6/2 mice. However, we did not observe any significant difference in the level of p-Akt in the PFC with Colivelin and dPEG-Colivelin treatments as compared to saline treated groups. Moreover, significant increase in p-JNK was observed in the ST and PFC of 40 mg/20g Colivelin treated R6/2 mice. Alternatively, we did not observe any behavioral improvements with Ceftriaxone or Sulforaphane.","abstract_has_math":false,"creators":["Ciesler, Jessica"],"institution":"University of Toledo Health Science Campus","degree_name":"Master of Science in Pharmaceutical Science (MSP)","degree_level":"masters","degree_discipline":"College of Pharmacy","degree_department":null,"school":null,"contributors":["Sari, Youssef"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2013,"date_issued":"2013-05-20","date_published":"2013-05-20","updated_at":"2026-07-24T03:37:16Z","subjects":["Pharmacology","Pharmacy Sciences","Neurosciences","Huntington's Disease","HD","Colivelin","dPEG-Colivelin","R6/2","Sulforaphane","Ceftriaxone"],"languages":["English"],"rights":["unrestricted","This thesis or dissertation is protected by copyright: all rights reserved. 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We hypothesized that the treatment of the R6/2 transgenic mouse model with neurotrophic peptides, Colivelin and analogue dPEG-Colivelin, Sulforaphane, a compound that reduces oxidative stress, and Ceftriaxone, a GLT-1 upregulator, would attenuate motor behavioral abnormalities and neurodegeneration in HD R6/2 mouse model.Although we did not observe any behavioral motor improvement with Colivelin and dPEG-Colivelin, we did, in fact, find significant up-regulation of p-Akt in the ST of 40 mg/20g Colivelin treated R6/2 mice as compared to saline treated R6/2 mice. However, we did not observe any significant difference in the level of p-Akt in the PFC with Colivelin and dPEG-Colivelin treatments as compared to saline treated groups. Moreover, significant increase in p-JNK was observed in the ST and PFC of 40 mg/20g Colivelin treated R6/2 mice. Alternatively, we did not observe any behavioral improvements with Ceftriaxone or Sulforaphane."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf","p.75","2.17 MB"]},{"key":"dc:title","label":"Title","values":["The Role of Trophic Factors and Other Drugs in the Treatment of Huntington's Disease in R6/2 Mouse Model"]}]}],"canonical_facts":{"dc:contributor":["Sari, Youssef"],"dc:creator":["Ciesler, Jessica"],"dc:date":["2013-05-20"],"dc:description":["Huntington's disease (HD) is a rare, autosomal dominant, neurodegenerative disease, characterized by behavioral and cognitive deterioration, as well as a progressive loss in motor control. HD is thought to be caused by the expansion of trinucleotide, CAG, expansion at the N-terminus within exon 1 of the huntingtin gene. The huntingtin protein is considered to play a role in the cell survival and apoptosis pathways of neurons, including Akt kinase and JNK. We hypothesized that the treatment of the R6/2 transgenic mouse model with neurotrophic peptides, Colivelin and analogue dPEG-Colivelin, Sulforaphane, a compound that reduces oxidative stress, and Ceftriaxone, a GLT-1 upregulator, would attenuate motor behavioral abnormalities and neurodegeneration in HD R6/2 mouse model.Although we did not observe any behavioral motor improvement with Colivelin and dPEG-Colivelin, we did, in fact, find significant up-regulation of p-Akt in the ST of 40 mg/20g Colivelin treated R6/2 mice as compared to saline treated R6/2 mice. However, we did not observe any significant difference in the level of p-Akt in the PFC with Colivelin and dPEG-Colivelin treatments as compared to saline treated groups. Moreover, significant increase in p-JNK was observed in the ST and PFC of 40 mg/20g Colivelin treated R6/2 mice. 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