Title |
Chronic overload of SEPT4, a parkin substrate that aggregates in Parkinson’s disease, causes behavioral alterations but not neurodegeneration in mice
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Published in |
Molecular Brain, August 2013
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DOI | 10.1186/1756-6606-6-35 |
Pubmed ID | |
Authors |
Natsumi Ageta-Ishihara, Hodaka Yamakado, Takao Morita, Satoko Hattori, Keizo Takao, Tsuyoshi Miyakawa, Ryosuke Takahashi, Makoto Kinoshita |
Abstract |
In autosomal recessive early-onset Parkinsonism (PARK2), the pathogenetic process from the loss of function of a ubiquitin ligase parkin to the death of dopamine neurons remains unclear. A dominant hypothesis attributes the neurotoxicity to accumulated substrates that are exempt from parkin-mediated degradation. Parkin substrates include two septins; SEPT4/CDCrel-2 which coaggregates with α-synuclein as Lewy bodies in Parkinson's disease, and its closest homolog SEPT5/CDCrel-1/PNUTL1 whose overload with viral vector can rapidly eliminate dopamine neurons in rats. However, chronic effects of pan-neural overload of septins have never been examined in mammals. To address this, we established a line of transgenic mice that express the largest gene product SEPT4(54kDa) via the prion promoter in the entire brain. |
X Demographics
Geographical breakdown
Country | Count | As % |
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Unknown | 1 | 100% |
Demographic breakdown
Type | Count | As % |
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Members of the public | 1 | 100% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Japan | 1 | 2% |
Unknown | 62 | 98% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Ph. D. Student | 11 | 17% |
Student > Doctoral Student | 6 | 10% |
Professor | 6 | 10% |
Researcher | 5 | 8% |
Student > Bachelor | 4 | 6% |
Other | 17 | 27% |
Unknown | 14 | 22% |
Readers by discipline | Count | As % |
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Biochemistry, Genetics and Molecular Biology | 10 | 16% |
Agricultural and Biological Sciences | 10 | 16% |
Medicine and Dentistry | 9 | 14% |
Neuroscience | 9 | 14% |
Physics and Astronomy | 3 | 5% |
Other | 5 | 8% |
Unknown | 17 | 27% |