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Lipid dysfunction and pathogenesis of multiple system atrophy

Overview of attention for article published in Acta Neuropathologica Communications, February 2014
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Title
Lipid dysfunction and pathogenesis of multiple system atrophy
Published in
Acta Neuropathologica Communications, February 2014
DOI 10.1186/2051-5960-2-15
Pubmed ID
Authors

Jonathan M Bleasel, Joanna H Wong, Glenda M Halliday, Woojin Scott Kim

Abstract

Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by the accumulation of α-synuclein protein in the cytoplasm of oligodendrocytes, the myelin-producing support cells of the central nervous system (CNS). The brain is the most lipid-rich organ in the body and disordered metabolism of various lipid constituents is increasingly recognized as an important factor in the pathogenesis of several neurodegenerative diseases. α-Synuclein is a 17 kDa protein with a close association to lipid membranes and biosynthetic processes in the CNS, yet its precise function is a matter of speculation, particularly in oligodendrocytes. α-Synuclein aggregation in neurons is a well-characterized feature of Parkinson's disease and dementia with Lewy bodies. Epidemiological evidence and in vitro studies of α-synuclein molecular dynamics suggest that disordered lipid homeostasis may play a role in the pathogenesis of α-synuclein aggregation. However, MSA is distinct from other α-synucleinopathies in a number of respects, not least the disparate cellular focus of α-synuclein pathology. The recent identification of causal mutations and polymorphisms in COQ2, a gene encoding a biosynthetic enzyme for the production of the lipid-soluble electron carrier coenzyme Q10 (ubiquinone), puts membrane transporters as central to MSA pathogenesis, although how such transporters are involved in the early myelin degeneration observed in MSA remains unclear. The purpose of this review is to bring together available evidence to explore the potential role of membrane transporters and lipid dyshomeostasis in the pathogenesis of α-synuclein aggregation in MSA. We hypothesize that dysregulation of the specialized lipid metabolism involved in myelin synthesis and maintenance by oligodendrocytes underlies the unique neuropathology of MSA.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 59 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 2%
Unknown 58 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 11 19%
Researcher 11 19%
Student > Bachelor 10 17%
Student > Master 4 7%
Other 2 3%
Other 8 14%
Unknown 13 22%
Readers by discipline Count As %
Medicine and Dentistry 13 22%
Neuroscience 7 12%
Biochemistry, Genetics and Molecular Biology 6 10%
Agricultural and Biological Sciences 5 8%
Pharmacology, Toxicology and Pharmaceutical Science 3 5%
Other 8 14%
Unknown 17 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 21 July 2022.
All research outputs
#15,708,506
of 23,342,232 outputs
Outputs from Acta Neuropathologica Communications
#1,168
of 1,418 outputs
Outputs of similar age
#192,400
of 310,089 outputs
Outputs of similar age from Acta Neuropathologica Communications
#18
of 37 outputs
Altmetric has tracked 23,342,232 research outputs across all sources so far. This one is in the 22nd percentile – i.e., 22% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,418 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 12th percentile – i.e., 12% 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 310,089 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 28th percentile – i.e., 28% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 37 others from the same source and published within six weeks on either side of this one. This one is in the 48th percentile – i.e., 48% of its contemporaries scored the same or lower than it.