# Dissecting neuroimmune response after axon injury

> **NIH NIH F32** · WASHINGTON UNIVERSITY · 2020 · $64,926

## Abstract

Inflammation, a function of the innate immune system, occurs in both acute and chronic neurodegenerative
conditions. However, we do not know how immune function is mechanistically related to neuronal maintenance
such as degeneration and regeneration. Sarm1 is a promising candidate in defining this mechanism. Sarm1 is
the central mediator of axon degeneration. Recently, Sarm1 was also found to be a factor of the innate
immune system. Yet, the function of Sarm1 in the immune response, and the effect of the immune response on
neuronal degeneration, remain unknown. This study will contribute to our mechanistic understanding of the
relationship between neuroimmune recruitment and neurodegeneration by elucidating the role of Sarm1,
through the following aims:
Aim 1: Define the Drosophila innate immune response to axon injury. Hemocytes, the innate immune
cells of Drosophila, interact with injured axons. But, the function of this interaction is unclear. I will correlate the
course of hemocyte recruitment with known events in axon degeneration and regeneration to identify a role for
the innate immune system during injury. I will also assess what defects in axonal injury and repair occur in the
absence of hemocytes.
Aim 2: Determine the role of Sarm1 in mediating neuroimmune response. I will determine if Sarm1 is
necessary and sufficient for hemocyte recruitment. I will then interrogate the molecular mechanism of Sarm1
mediated immune recruitment by manipulating the enzymatic activity of Sarm1, which has recently been shown
to be required for immune response in plants.
Aim 3: Identify innate immune messengers and pathways activated by axonal injury. To determine the
mechanism mediating immune recruitment to injured neurons, I will identify cytokines and downstream
signaling pathways required for neuroimmune interaction after injury.
Successful completion of this proposal will bridge gaps in knowledge relating to the initiation of
neuroimmune recruitment during axon degeneration.

## Key facts

- **NIH application ID:** 10044023
- **Project number:** 1F32NS117784-01
- **Recipient organization:** WASHINGTON UNIVERSITY
- **Principal Investigator:** Laura Devault
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $64,926
- **Award type:** 1
- **Project period:** 2020-09-01 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10044023

## Citation

> US National Institutes of Health, RePORTER application 10044023, Dissecting neuroimmune response after axon injury (1F32NS117784-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10044023. Licensed CC0.

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