# Macrophages in homeostasis and cardiovascular disease

> **NIH NIH R35** · MASSACHUSETTS GENERAL HOSPITAL · 2020 · $358,800

## Abstract

Alzheimer's disease (AD) is a chronic neurodegenerative disease and a major cause of
dementia. While early symptoms include short term memory loss, as the disease advances,
symptoms progressively worsen and include cognitive decline, disorientation, and ultimately
loss of body function and death. The disease involves accumulation of plaques in the brain,
which are characterized by the deposition of a protein called amyloid-β (Aβ). Relatively recent
research has shown that the immune system is an important component of AD. Specifically,
interspersed throughout the brain among and between the neurons are immune cells called
microglia that reside in the brain throughout life and participate in many normal functions, but
can also be critical in AD. Understanding microglia in AD, is therefore necessary, as it may
uncover previously unknown pathways by which the immune system promotes or protects
against AD. A powerful strategy to delve into microglial function involves identifying the key
molecules that control microglial development, survival, and behavior. For this application, we
have generated preliminary data suggesting that a specific molecule, a growth factor and
cytokine called IL-3 is protective in AD. We show that a cluster of immune cells called
astrocytes inhabiting specific locations of the brain produce IL-3, which then activates
microglial cells, instructing them to remove the harmful amyloid-β (Aβ) plaques. In the absence
of IL-3, however, microglia are unable to find amyloid-β (Aβ) plaques, which worsens disease.
IL-3, therefore, might be an important therapeutic in AD. This application will focus on the role
of microglial-astrocyte communication in AD.

## Key facts

- **NIH application ID:** 10128792
- **Project number:** 3R35HL135752-04S1
- **Recipient organization:** MASSACHUSETTS GENERAL HOSPITAL
- **Principal Investigator:** Filip K Swirski
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $358,800
- **Award type:** 3
- **Project period:** 2017-03-01 → 2024-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10128792

## Citation

> US National Institutes of Health, RePORTER application 10128792, Macrophages in homeostasis and cardiovascular disease (3R35HL135752-04S1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10128792. Licensed CC0.

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