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Accumulation of α-synuclein in dementia with Lewy bodies is associated with decline in the α-synuclein-degrading enzymes kallikrein-6 and calpain-1

Overview of attention for article published in Acta Neuropathologica Communications, December 2014
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  • Above-average Attention Score compared to outputs of the same age (51st percentile)
  • Good Attention Score compared to outputs of the same age and source (73rd percentile)

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Title
Accumulation of α-synuclein in dementia with Lewy bodies is associated with decline in the α-synuclein-degrading enzymes kallikrein-6 and calpain-1
Published in
Acta Neuropathologica Communications, December 2014
DOI 10.1186/s40478-014-0164-0
Pubmed ID
Authors

J Scott Miners, Ruth Renfrew, Marta Swirski, Seth Love

Abstract

Kallikrein-6 and calpain-1 are amongst a small group of proteases that degrade ¿-synuclein. We have explored the possibility that reduction in the level or activity of these enzymes contributes to the accumulation of ¿-synuclein in Lewy body diseases. We measured calpain-1 activity by fluorogenic activity assay, kallikrein-6 level by sandwich ELISA, and levels of ¿-synuclein and ¿-synuclein phosphorylated at serine 129 (¿-synuclein-P129), in post-mortem brain tissue in pure dementia with Lewy bodies (DLB, n = 12), Alzheimer¿s disease (AD, n = 20) and age-matched controls (n = 19). Calpain-1 activity was significantly reduced in DLB within the cingulate and parahippocampal cortex, regions with highest ¿-synuclein and ¿-synuclein-P129 load, and correlated inversely with the levels of ¿-synuclein and ¿-synuclein-P129. Calpain-1 was unaltered in the thalamus and frontal cortex, regions with less ¿-synuclein pathology. Kallikrein-6 level was reduced in the cingulate cortex in the DLB cohort, and correlated inversely with ¿-synuclein and ¿-synuclein-P129. Kallikrein-6 was also reduced in DLB in the thalamus but not in relation to ¿-synuclein or ¿-synuclein-P129 load and was unaltered in the frontal and parahippocampal cortex. In SH-SY5Y cells overexpressing wild-type ¿-synuclein there was partial co-localisation of kallikrein-6 and calpain-1 with ¿-synuclein, and siRNA-mediated knock-down of kallikrein-6 and calpain-1 increased the amount of ¿-synuclein in cell lysates. Our results indicate that reductions in kallikrein-6 and calpain-1 may contribute to the accumulation of ¿-synuclein in DLB.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 40 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 1 3%
Unknown 39 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 23%
Student > Bachelor 5 13%
Other 5 13%
Student > Master 5 13%
Researcher 4 10%
Other 7 18%
Unknown 5 13%
Readers by discipline Count As %
Agricultural and Biological Sciences 11 28%
Neuroscience 9 23%
Biochemistry, Genetics and Molecular Biology 6 15%
Pharmacology, Toxicology and Pharmaceutical Science 1 3%
Psychology 1 3%
Other 3 8%
Unknown 9 23%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. 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 19 September 2015.
All research outputs
#13,184,450
of 22,772,779 outputs
Outputs from Acta Neuropathologica Communications
#1,004
of 1,371 outputs
Outputs of similar age
#173,257
of 359,774 outputs
Outputs of similar age from Acta Neuropathologica Communications
#5
of 19 outputs
Altmetric has tracked 22,772,779 research outputs across all sources so far. This one is in the 41st percentile – i.e., 41% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,371 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 12.8. This one is in the 26th percentile – i.e., 26% 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 359,774 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 51% of its contemporaries.
We're also able to compare this research output to 19 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 73% of its contemporaries.