Acupuncture Inhibits the Increase in Alpha-Synuclein in Substantia Nigra in an MPTP- Induced Parkinsonism Mouse Model

Parkinson’s disease, a progressive neurodegenerative disease, is caused by the loss of dopaminergic neurons in the substantia nigra (SN). It is characterized by the formation of intracytoplasmic Lewy bodies that are primarily composed of the protein alpha-synuclein (α-syn), along with dystrophic neu...

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Published inAdvances in experimental medicine and biology Vol. 1232; pp. 401 - 408
Main Authors Yeo, Sujung, Song, Jongbeom, Lim, Sabina
Format Book Chapter Journal Article
LanguageEnglish
Published Cham Springer International Publishing 2020
SeriesAdvances in Experimental Medicine and Biology
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ISBN3030344592
9783030344597
ISSN0065-2598
2214-8019
DOI10.1007/978-3-030-34461-0_51

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Summary:Parkinson’s disease, a progressive neurodegenerative disease, is caused by the loss of dopaminergic neurons in the substantia nigra (SN). It is characterized by the formation of intracytoplasmic Lewy bodies that are primarily composed of the protein alpha-synuclein (α-syn), along with dystrophic neurites. Acupuncture stimulation results in an enhanced survival of dopaminergic neurons in the SN in Parkinsonism animal models. We investigated the role of acupuncture in inhibiting the increase in α-syn expression that is related to dopaminergic cell loss in the SN in a chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) Parkinsonism mouse model. In this model, acupuncture stimulation at GB34 and LR3 attenuated the decrease in tyrosine hydroxylase in the SN. Moreover, acupuncture stimulation attenuated the increase in α-syn in SN. Acupuncture stimulation also maintained the phosphorylated α-syn on serine 129 at levels similar to the control group. Our findings indicate that the MPTP-mediated increase in α-syn, and the acupuncture-mediated inhibition of the increase in α-syn, may be responsible for the neuroprotective effects of acupuncture in the SN following damage induced by MPTP.
ISBN:3030344592
9783030344597
ISSN:0065-2598
2214-8019
DOI:10.1007/978-3-030-34461-0_51