Document Type
Article
Publication Date
11-20-2019
Keywords
JMG
JAX Source
Neuron 2019 Nov 20; 104(4):637-653
Volume
104
Issue
4
First Page
637
Last Page
653
ISSN
1097-4199
PMID
31751545
DOI
https://doi.org/10.1016/j.neuron.2019.09.018
Grant
DA039841
Abstract
Neuropathic pain (NeuP) arises due to injury of the somatosensory nervous system and is both common and disabling, rendering an urgent need for non-addictive, effective new therapies. Given the high evolutionary conservation of pain, investigative approaches from Drosophila mutagenesis to human Mendelian genetics have aided our understanding of the maladaptive plasticity underlying NeuP. Successes include the identification of ion channel variants causing hyper-excitability and the importance of neuro-immune signaling. Recent developments encompass improved sensory phenotyping in animal models and patients, brain imaging, and electrophysiology-based pain biomarkers, the collection of large well-phenotyped population cohorts, neurons derived from patient stem cells, and high-precision CRISPR generated genetic editing. We will discuss how to harness these resources to understand the pathophysiological drivers of NeuP, define its relationship with comorbidities such as anxiety, depression, and sleep disorders, and explore how to apply these findings to the prediction, diagnosis, and treatment of NeuP in the clinic.
Recommended Citation
Calvo M,
Davies A,
Hébert H,
Weir G,
Chesler E,
Finnerup N,
Levitt R,
Smith B,
Neely G,
Costigan M,
Bennett D.
The Genetics of Neuropathic Pain from Model Organisms to Clinical Application. Neuron 2019 Nov 20; 104(4):637-653
Comments
This open access article is licensed under a Creative Commons Attribution 4.0 International License.