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Wallerian degeneration: gaining perspective on inflammatory events after peripheral nerve injury

Overview of attention for article published in Journal of Neuroinflammation, January 2011
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (80th percentile)

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1 patent
1 Facebook page
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724 Mendeley
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Wallerian degeneration: gaining perspective on inflammatory events after peripheral nerve injury
Published in
Journal of Neuroinflammation, January 2011
DOI 10.1186/1742-2094-8-110
Pubmed ID

Andrew D Gaudet, Phillip G Popovich, Matt S Ramer


In this review, we first provide a brief historical perspective, discussing how peripheral nerve injury (PNI) may have caused World War I. We then consider the initiation, progression, and resolution of the cellular inflammatory response after PNI, before comparing the PNI inflammatory response with that induced by spinal cord injury (SCI).In contrast with central nervous system (CNS) axons, those in the periphery have the remarkable ability to regenerate after injury. Nevertheless, peripheral nervous system (PNS) axon regrowth is hampered by nerve gaps created by injury. In addition, the growth-supportive milieu of PNS axons is not sustained over time, precluding long-distance regeneration. Therefore, studying PNI could be instructive for both improving PNS regeneration and recovery after CNS injury. In addition to requiring a robust regenerative response from the injured neuron itself, successful axon regeneration is dependent on the coordinated efforts of non-neuronal cells which release extracellular matrix molecules, cytokines, and growth factors that support axon regrowth. The inflammatory response is initiated by axonal disintegration in the distal nerve stump: this causes blood-nerve barrier permeabilization and activates nearby Schwann cells and resident macrophages via receptors sensitive to tissue damage. Denervated Schwann cells respond to injury by shedding myelin, proliferating, phagocytosing debris, and releasing cytokines that recruit blood-borne monocytes/macrophages. Macrophages take over the bulk of phagocytosis within days of PNI, before exiting the nerve by the circulation once remyelination has occurred. The efficacy of the PNS inflammatory response (although transient) stands in stark contrast with that of the CNS, where the response of nearby cells is associated with inhibitory scar formation, quiescence, and degeneration/apoptosis. Rather than efficiently removing debris before resolving the inflammatory response as in other tissues, macrophages infiltrating the CNS exacerbate cell death and damage by releasing toxic pro-inflammatory mediators over an extended period of time. Future research will help determine how to manipulate PNS and CNS inflammatory responses in order to improve tissue repair and functional recovery.

Mendeley readers

The data shown below were compiled from readership statistics for 724 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 7 <1%
Chile 3 <1%
Portugal 2 <1%
Mexico 2 <1%
Germany 1 <1%
United Kingdom 1 <1%
Brazil 1 <1%
Czechia 1 <1%
Canada 1 <1%
Other 0 0%
Unknown 705 97%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 148 20%
Student > Bachelor 113 16%
Student > Master 96 13%
Researcher 86 12%
Student > Doctoral Student 55 8%
Other 118 16%
Unknown 108 15%
Readers by discipline Count As %
Agricultural and Biological Sciences 157 22%
Medicine and Dentistry 149 21%
Neuroscience 128 18%
Biochemistry, Genetics and Molecular Biology 47 6%
Engineering 40 6%
Other 75 10%
Unknown 128 18%

Attention Score in Context

This research output has an Altmetric Attention Score of 7. 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 03 March 2022.
All research outputs
of 21,047,241 outputs
Outputs from Journal of Neuroinflammation
of 2,437 outputs
Outputs of similar age
of 141,690 outputs
Outputs of similar age from Journal of Neuroinflammation
of 2 outputs
Altmetric has tracked 21,047,241 research outputs across all sources so far. Compared to these this one has done well and is in the 80th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,437 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.1. This one has gotten more attention than average, scoring higher than 63% of its peers.
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 141,690 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 80% of its contemporaries.
We're also able to compare this research output to 2 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them