Targeting AMPK for Neuropathic Pain Treatment
Author Information
Author(s): Melemedjian Ohannes K, Asiedu Marina N, Tillu Dipti V, Sanoja Raul, Yan Jin, Lark Arianna, Khoutorsky Arkady, Johnson Jessica, Peebles Katherine A, Lepow Talya, Sonenberg Nahum, Dussor Gregory, Price Theodore J
Primary Institution: University of Arizona
Hypothesis
Dysregulated translation regulation pathways may underlie neuropathic pain.
Conclusion
AMPK activation can reverse neuropathic allodynia and decrease sensory neuron excitability.
Supporting Evidence
- PNI leads to changes in sensory neuron function resulting in hyperexcitability.
- Metformin and A769662 reversed tactile allodynia in preclinical models.
- AMPK activation normalizes aberrant gene expression at the level of translation.
Takeaway
This study shows that a drug called metformin can help reduce pain by changing how nerve cells make proteins.
Methodology
The study used rat and mouse models of neuropathic pain to assess biochemical changes and the effects of AMPK activators.
Limitations
The study is preclinical and may not directly translate to human conditions.
Participant Demographics
Male ICR mice and male Sprague Dawley rats were used.
Statistical Information
P-Value
0.001
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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