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Dorsal root ganglia in Friedreich ataxia: satellite cell proliferation and inflammation

Overview of attention for article published in Acta Neuropathologica Communications, May 2016
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Title
Dorsal root ganglia in Friedreich ataxia: satellite cell proliferation and inflammation
Published in
Acta Neuropathologica Communications, May 2016
DOI 10.1186/s40478-016-0288-5
Pubmed ID
Authors

Arnulf H. Koeppen, R. Liane Ramirez, Alyssa B. Becker, Joseph E. Mazurkiewicz

Abstract

Dorsal root ganglia (DRG) are highly vulnerable to frataxin deficiency in Friedreich ataxia (FA), an autosomal recessive disease due to pathogenic homozygous guanine-adenine-adenine trinucleotide repeat expansions in intron 1 of the FXN gene (chromosome 9q21.11). An immunohistochemical and immunofluorescence study of DRG in 15 FA cases and 12 controls revealed that FA causes major primary changes in satellite cells and inflammatory destruction of neurons. A panel of antibodies was used to reveal the cytoplasm of satellite cells (glutamine synthetase, S100, metabotropic glutamate receptors 2/3, excitatory amino acid transporter 1, ATP-sensitive inward rectifier potassium channel 10, and cytosolic ferritin), gap junctions (connexin 43), basement membranes (laminin), mitochondria (ATP synthase subunit beta and frataxin), and monocytes (CD68 and IBA1). Reaction product of the cytoplasmic markers and laminin confirmed proliferation of satellite cells and processes into multiple perineuronal layers and residual nodules. The formation of connexin 43-reactive gap junctions between satellite cells was strongly upregulated. Proliferating satellite cells in FA displayed many more frataxin- and ATP5B-reactive mitochondria than normal. Monocytes entered into the satellite cell layer, appeared to penetrate neuronal plasma membranes, and infiltrated residual nodules. Satellite cells and IBA1-reactive monocytes displayed upregulated ferritin biosynthesis, which was most likely due to leakage of iron from dying neurons. We conclude that FA differentially affects the key cellular elements of DRG, and postulate that the disease causes loss of bidirectional trophic support between satellite cells and neurons.

Twitter Demographics

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Mendeley readers

The data shown below were compiled from readership statistics for 46 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 46 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 11 24%
Student > Master 9 20%
Student > Bachelor 4 9%
Student > Doctoral Student 4 9%
Student > Postgraduate 4 9%
Other 10 22%
Unknown 4 9%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 14 30%
Neuroscience 8 17%
Medicine and Dentistry 7 15%
Agricultural and Biological Sciences 4 9%
Veterinary Science and Veterinary Medicine 1 2%
Other 4 9%
Unknown 8 17%

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 07 May 2016.
All research outputs
#3,744,956
of 7,662,843 outputs
Outputs from Acta Neuropathologica Communications
#233
of 360 outputs
Outputs of similar age
#133,150
of 266,510 outputs
Outputs of similar age from Acta Neuropathologica Communications
#24
of 33 outputs
Altmetric has tracked 7,662,843 research outputs across all sources so far. This one is in the 48th percentile – i.e., 48% of other outputs scored the same or lower than it.
So far Altmetric has tracked 360 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.2. This one is in the 32nd percentile – i.e., 32% 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 266,510 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 46th percentile – i.e., 46% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 33 others from the same source and published within six weeks on either side of this one. This one is in the 24th percentile – i.e., 24% of its contemporaries scored the same or lower than it.