Loss of autophagy in dopaminergic neurons causes Lewy pathology and motor dysfunction in aged mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Shigeto Sato, Toshiki Uchihara, Takahiro Fukuda, Sachiko Noda, Hiromi Kondo, Shinji Saiki, Masaaki Komatsu, Yasuo Uchiyama, Keiji Tanaka, Nobutaka Hattori

ABSTRACT

Inactivation of constitutive autophagy results in the formation of cytoplasmic inclusions in neurons, but the relationship between impaired autophagy and Lewy bodies (LBs) as well as the in vivo process of formation remains unknown. Synuclein, a component of LBs, is the defining characteristic of Parkinson's disease (PD). Here, we characterize dopamine (DA) neuron-specific autophagy-deficient mice and provide in vivo evidence for LB formation. Synuclein deposition is preceded by p62 and resulted in the formation of inclusions containing synuclein and p62. The number and size of these inclusions were gradually increased in neurites rather than soma with aging. These inclusions may facilitate peripheral failures. As a result, DA neuron loss and motor dysfunction including the hindlimb defect were observed in 120-week-old mice. P62 aggregates derived from an autophagic defect might serve as "seeds" and can potentially be cause of LB formation. More... »

PAGES

2813

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-018-21325-w

DOI

http://dx.doi.org/10.1038/s41598-018-21325-w

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1100868130

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29434298


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34 schema:description Inactivation of constitutive autophagy results in the formation of cytoplasmic inclusions in neurons, but the relationship between impaired autophagy and Lewy bodies (LBs) as well as the in vivo process of formation remains unknown. Synuclein, a component of LBs, is the defining characteristic of Parkinson's disease (PD). Here, we characterize dopamine (DA) neuron-specific autophagy-deficient mice and provide in vivo evidence for LB formation. Synuclein deposition is preceded by p62 and resulted in the formation of inclusions containing synuclein and p62. The number and size of these inclusions were gradually increased in neurites rather than soma with aging. These inclusions may facilitate peripheral failures. As a result, DA neuron loss and motor dysfunction including the hindlimb defect were observed in 120-week-old mice. P62 aggregates derived from an autophagic defect might serve as "seeds" and can potentially be cause of LB formation.
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