# AIF1/Iba1 in microglial function and stroke

> **NIH NIH R21** · ALBERT EINSTEIN COLLEGE OF MEDICINE · 2020 · $440,623

## Abstract

Abstract
Every year, nearly 800,000 people in the United States suffer a stroke, a major cause of
mortality and the leading preventable cause of disability. Most of these incidents are
first-time strokes, and nearly 9 out of 10 strokes can be classified as ischemic in
etiology. Such strokes occur when a clot or a mass blocks an artery supplying part of the
brain, cutting off blood flow and often leading to permanent neuronal injury.
Microglia are brain-resident cells of the macrophage lineage that activate rapidly in
response to a variety of stimuli and injuries, including ischemic stroke. Upon activation,
microglia undergo morphological changes, increase expression of markers including
CD68 and major histocompatibility complex class II, and produce pro-inflammatory
cytokines such as tumor necrosis factor-ɑ (TNF-ɑ) and interleukin-6 (IL-6). Activated
microglia are commonly observed in many brain diseases in addition to stroke, including
Alzheimer's and Parkinson's diseases, and are regarded as key mediators of neuro-
inflammation. How microglial activation affects brain injury is complex, since they can
mediate both beneficial and detrimental effects, protecting neurons by removing
apoptotic cells and debris via phagocytic processes, or potentially contributing to injury
through their pro-inflammatory activities.
Allograft inflammatory factor-1 (AIF1, also known as Iba1) is a highly conserved 17kD
Ca2+ binding protein expressed in microglia and upregulated in response to neural injury.
While AIF1/Iba1 is widely used as a marker of microglia, its specific contributions to
microglia homeostasis and activation are not well understood. We have generated both
global and conditional alleles to inactivate AIF1/Iba1 expression in mice; preliminary
studies suggest notably larger areas of stroke injury in mice lacking AIF1/Iba1. In this
proposal, we will use loss of function studies to assess the in vivo contribution of
AIF1/Iba1 to basic microglial functions, such as migration and phagocytosis, which are
important for response to neural injury. We will also determine how loss of AIF1/Iba1
affects the integrated in vivo response in a mouse model of ischemic stroke. These
studies will add to our understanding of microglial function in stroke recovery, and
characterize how AIF1/Iba1 contributes to recovery in this setting.

## Key facts

- **NIH application ID:** 10057671
- **Project number:** 1R21NS116480-01A1
- **Recipient organization:** ALBERT EINSTEIN COLLEGE OF MEDICINE
- **Principal Investigator:** Sayan Nandi
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $440,623
- **Award type:** 1
- **Project period:** 2020-07-01 → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10057671

## Citation

> US National Institutes of Health, RePORTER application 10057671, AIF1/Iba1 in microglial function and stroke (1R21NS116480-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10057671. Licensed CC0.

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