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| Funder | Swedish Research Council |
|---|---|
| Recipient Organization | Linköping University |
| Country | Sweden |
| Start Date | Jan 01, 2025 |
| End Date | Dec 31, 2027 |
| Duration | 1,094 days |
| Number of Grantees | 3 |
| Roles | Co-Investigator; Principal Investigator |
| Data Source | Swedish Research Council |
| Grant ID | 2024-02781_VR |
The inflammatory response is a natural reaction to harm or infection and facilitates a healing environment.
However, in some cases, the inflammatory state doesn’t resolve properly, leading through immune and neurological mechanisms to chronic pain, even though the initial causal factors are no longer present.
Despite ongoing efforts, the mechanisms by which different types of peripheral sensory neurons contribute to the development and maintenance of chronic pain remain unclear.
One reason for this knowledge gap is that molecular and functional analyses often offer fragmented perspective of the systemic mechanisms involved.
To bridge this gap, we have developed a unique methodology that enables simultaneous high-throughput functional and genetic characterization of peripheral sensory neurons activity.
Leveraging this, we aim to uncover the mechanisms behind global and cell-type specific changes in stimuli representation induced by cutaneous and deep inflammation.
Thanks to close ongoing collaboration with clinically oriented groups we will be able to interpret our insights in translational framework.
Ultimately, we anticipate identifying neuronal cell classes pivotal in the shift from acute to chronic pain and delineating the genetic pathways responsible for these transitions.
Linköping University
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