You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output.
Click here to find out more.
X Demographics
Mendeley readers
Attention Score in Context
| Title |
PARK14 (D331Y) PLA2G6 Causes Early-Onset Degeneration of Substantia Nigra Dopaminergic Neurons by Inducing Mitochondrial Dysfunction, ER Stress, Mitophagy Impairment and Transcriptional Dysregulation in a Knockin Mouse Model
|
|---|---|
| Published in |
Molecular Neurobiology, August 2018
|
| DOI | 10.1007/s12035-018-1118-5 |
| Pubmed ID | |
| Authors |
Ching-Chi Chiu, Chin-Song Lu, Yi-Hsin Weng, Ying-Ling Chen, Ying-Zu Huang, Rou-Shayn Chen, Yi-Chuan Cheng, Yin-Cheng Huang, Yu-Chuan Liu, Szu-Chia Lai, Kun-Jun Lin, Yan-Wei Lin, Yu-Jie Chen, Chao-Lang Chen, Tu-Hsueh Yeh, Hung-Li Wang |
| Abstract |
PARK14 patients with homozygous (D331Y) PLA2G6 mutation display motor deficits of pure early-onset Parkinson's disease (PD). The aim of this study is to investigate the pathogenic mechanism of mutant (D331Y) PLA2G6-induced PD. We generated knockin (KI) mouse model of PARK14 harboring homozygous (D331Y) PLA2G6 mutation. Then, we investigated neuropathological and neurological phenotypes of PLA2G6D331Y/D331Y KI mice and molecular pathogenic mechanisms of (D331Y) PLA2G6-induced degeneration of substantia nigra (SN) dopaminergic neurons. Six-or nine-month-old PLA2G6D331Y/D331Y KI mice displayed early-onset cell death of SNpc dopaminergic neurons. Lewy body pathology was found in the SN of PLA2G6D331Y/D331Y mice. Six-or nine-month-old PLA2G6D331Y/D331Y KI mice exhibited early-onset parkinsonism phenotypes. Disrupted cristae of mitochondria were found in SNpc dopaminergic neurons of PLA2G6D331Y/D331Y mice. PLA2G6D331Y/D331Y mice displayed mitochondrial dysfunction and upregulated ROS production, which may lead to activation of apoptotic cascade. Upregulated protein levels of Grp78, IRE1, PERK, and CHOP, which are involved in activation of ER stress, were found in the SN of PLA2G6D331Y/D331Y mice. Protein expression of mitophagic proteins, including parkin and BNIP3, was downregulated in the SN of PLA2G6D331Y/D331Y mice, suggesting that (D331Y) PLA2G6 mutation causes mitophagy dysfunction. In the SN of PLA2G6D331Y/D331Y mice, mRNA levels of eight genes that are involved in neuroprotection/neurogenesis were decreased, while mRNA levels of two genes that promote apoptotic death were increased. Our results suggest that PARK14 (D331Y) PLA2G6 mutation causes degeneration of SNpc dopaminergic neurons by causing mitochondrial dysfunction, elevated ER stress, mitophagy impairment, and transcriptional abnormality. |
X Demographics
The data shown below were collected from the profiles of 6 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| United States | 2 | 33% |
| France | 1 | 17% |
| Unknown | 3 | 50% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 4 | 67% |
| Science communicators (journalists, bloggers, editors) | 1 | 17% |
| Scientists | 1 | 17% |
Mendeley readers
The data shown below were compiled from readership statistics for 52 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 52 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Bachelor | 7 | 13% |
| Researcher | 5 | 10% |
| Student > Master | 4 | 8% |
| Student > Doctoral Student | 3 | 6% |
| Professor | 3 | 6% |
| Other | 8 | 15% |
| Unknown | 22 | 42% |
| Readers by discipline | Count | As % |
|---|---|---|
| Neuroscience | 9 | 17% |
| Medicine and Dentistry | 6 | 12% |
| Agricultural and Biological Sciences | 5 | 10% |
| Biochemistry, Genetics and Molecular Biology | 4 | 8% |
| Computer Science | 1 | 2% |
| Other | 0 | 0% |
| Unknown | 27 | 52% |
Attention Score in Context
This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 30 August 2019.
All research outputs
#14,138,420
of 23,099,576 outputs
Outputs from Molecular Neurobiology
#1,781
of 3,499 outputs
Outputs of similar age
#179,592
of 331,157 outputs
Outputs of similar age from Molecular Neurobiology
#60
of 126 outputs
Altmetric has tracked 23,099,576 research outputs across all sources so far. This one is in the 37th percentile – i.e., 37% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,499 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.2. This one is in the 47th percentile – i.e., 47% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 331,157 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 44th percentile – i.e., 44% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 126 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 50% of its contemporaries.