# Neuroinflammation as a Theraputic Avenue for Alzheimer's Disease Treatment

> **NIH NIH F32** · UNIVERSITY OF ARIZONA · 2020 · $22,546

## Abstract

Abstract
Title: Neuroinflammation as a therapeutic avenue for Alzheimer's disease treatment
The role of neuroinflammation in neurological disorders remains controversial. While triggered by the toxic
accumulation of Aβ, Alzheimer's disease (AD) is thought to be potentiated by blood-brain barrier (BBB)
breakdown and immune cell infiltration to the brain. However, drugs that inhibit immune cell infiltration to the
CNS have failed as treatments for AD. In other disease models, like infection with the neurotropic parasite
Toxoplasma gondii, neuroinflammation is required for survival of both mice and humans, yet almost all of the
infected population (over 2 billion people worldwide) harbors a life-long asymptomatic infection. Thus, T. gondii
infection models an immune response that is robust to control the parasite yet tightly controlled prevent
immune mediated pathology in the brain. Our lab has discovered that of the three canonical T. gondii strains,
infection with type II parasites protects against Aβ deposition in the brain. Though prolonged inflammation has
been shown to promote alternative activation in monocyte lineage cell types, data generated in our lab shows
that type II parasites induce a larger population of alternatively activated macrophages in the brain. Therefore, I
hypothesize that infection with type II parasites generates a population of phagocytic, alternatively
activated macrophages that can more easily access the brain and clear β-amyloid plaques. To test this
hypothesis, I will determine the impact type II infection has on the BBB, Aβ clearance from the brain and the
populations of immune cells that infiltrate the CNS compared to infection with type III parasites. This strategy
will allow me to quickly separate changes in the brain that aid specifically in Aβ clearance from changes that
occur during infection in general. Identifying the cell types that are capable of eliminating pathogenic plaques
from the brain would lead to new strategies to combat the toxic accumulation Aβ.

## Key facts

- **NIH application ID:** 9869828
- **Project number:** 5F32AG058440-03
- **Recipient organization:** UNIVERSITY OF ARIZONA
- **Principal Investigator:** Kathryn Elizabeth McGovern
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $22,546
- **Award type:** 5
- **Project period:** 2018-03-01 → 2020-06-18

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9869828

## Citation

> US National Institutes of Health, RePORTER application 9869828, Neuroinflammation as a Theraputic Avenue for Alzheimer's Disease Treatment (5F32AG058440-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9869828. Licensed CC0.

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