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dc.contributor.authorPark, Mijeong-
dc.contributor.authorHa, Jimin-
dc.contributor.authorLee, Yuri-
dc.contributor.authorChoi, Hoon-Seong-
dc.contributor.authorKim, Byoung Soo-
dc.contributor.authorJeong, Youn Kyoung-
dc.date.accessioned2024-01-12T06:31:52Z-
dc.date.available2024-01-12T06:31:52Z-
dc.date.created2023-09-19-
dc.date.issued2023-12-
dc.identifier.issn0197-4580-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/79721-
dc.description.abstractThe anti-inflammatory efficacy of radiation therapy (RT) with single fractions below 1.0 Gy has been demonstrated in Alzheimer’s disease mouse models. As neuroinflammation is also a major pathological feature of Parkinson’s disease (PD), RT may also be effective in PD treatment. Therefore, this study aimed to investigate the anti-inflammatory effect of low-moderate dose RT (LMDRT, 0.6 Gy/single dose, for 5 days) exposure in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 30 mg/kg, i.p., for 5 consecutive days)-induced PD mouse model. Importantly, LMDRT reduced the levels of glial fibrillary acidic protein (GFAP) and intercellular adhesion molecule-1 (ICAM-1, CD54) in the striatum region, which increased following MPTP administration. LMDRT also modulated inflammatory gene expression patterns in the substantia nigra region of the MPTP-treated mice. However, LMDRT had no direct effects on the severe loss of dopaminergic neurons and impaired motor behavior in the rotarod test. These results indicate that LMDRT has anti-inflammatory effects by modulating neuroinflammatory factors, including GFAP and ICAM-1, but showed no behavioral improvements or neuroprotection in the MPTP-induced mouse model of PD.-
dc.languageEnglish-
dc.publisherElsevier BV-
dc.titleLow-moderate dose whole-brain γ-ray irradiation modulates the expressions of GFAP and ICAM-1 in the MPTP-induced Parkinson’s disease mouse model-
dc.typeArticle-
dc.identifier.doi10.1016/j.neurobiolaging.2023.06.015-
dc.description.journalClass1-
dc.identifier.bibliographicCitationNeurobiology of Aging, v.132, pp.175 - 184-
dc.citation.titleNeurobiology of Aging-
dc.citation.volume132-
dc.citation.startPage175-
dc.citation.endPage184-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid001106776400001-
dc.relation.journalWebOfScienceCategoryGeriatrics & Gerontology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalResearchAreaGeriatrics & Gerontology-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.type.docTypeArticle-
dc.subject.keywordPlusRADIATION-THERAPY-
dc.subject.keywordPlusSUBACUTE MPTP-
dc.subject.keywordPlusANIMAL-MODEL-
dc.subject.keywordPlusNEUROINFLAMMATION-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusLEVODOPA-
dc.subject.keywordPlusICAM-1-
dc.subject.keywordPlusMICE-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordAuthorLow-moderate dose radiation therapy-
dc.subject.keywordAuthorParkinson&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorNeuroinflammation-
dc.subject.keywordAuthorGFAP-
dc.subject.keywordAuthorICAM-1 (CD54)-
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