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L-DOPA regulates neuroinflammation and Aβ pathology through NEP and ADAM17 in a mouse model of ADopen access

Authors
Lee, Hyun-juNam, JinhanHwang, Jeong-WooPark, Jin-HeeJeong, Yoo JooJang, Ji-YeongKim, Su-JeongJo, A-RanHoe, Hyang-Sook
Issue Date
Apr-2024
Publisher
BMC
Keywords
L-DOPA; A beta; Tau; Neuroinflammation; Alzheimer's disease
Citation
MOLECULAR BRAIN, v.17, no.1
Journal Title
MOLECULAR BRAIN
Volume
17
Number
1
URI
http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/1172
DOI
10.1186/s13041-024-01092-8
ISSN
1756-6606
Abstract
Dopamine plays important roles in cognitive function and inflammation and therefore is involved in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). Drugs that increase or maintain dopamine levels in the brain could be a therapeutic strategy for AD. However, the effects of dopamine and its precursor levodopa (L-DOPA) on A beta/tau pathology in vivo and the underlying molecular mechanisms have not been studied in detail. Here, we investigated whether L-DOPA treatment alters neuroinflammation, A beta pathology, and tau phosphorylation in 5xFAD mice, a model of AD. We found that L-DOPA administration significantly reduced microgliosis and astrogliosis in 5xFAD mice. In addition, L-DOPA treatment significantly decreased A beta plaque number by upregulating NEP and ADAM17 levels in 5xFAD mice. However, L-DOPA-treated 5xFAD mice did not exhibit changes in tau hyperphosphorylation or tau kinase levels. These data suggest that L-DOPA alleviates neuroinflammatory responses and A beta pathology but not tau pathology in this mouse model of AD.
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연구본부 (퇴행성뇌질환 연구그룹)
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