# Novel mechanism controlling calcium signaling to treat and prevent neurodegeneration in early stage glaucoma

> **NIH NIH R01** · UNIVERSITY OF MISSOURI KANSAS CITY · 2021 · $391,250

## Abstract

PROJECT SUMMARY / ABSTRACT
The present administrative supplement application responds to NOT-AG-20-034, “Notice of
Special Interest: Alzheimer's-focused administrative supplements for NIH grants that are not
focused on Alzheimer's disease”. Under the parent grant for the present administrative
supplement, R01 grant 1R01EY031248-01, entitled “Novel mechanism controlling calcium
signaling to treat and prevent neurodegeneration in early stage glaucoma”, we are targeting a
novel signaling pathway for the development of a novel pharmacological intervention to control
degeneration of nerve cells in the retina and optic nerve due to glaucoma, a major cause of
visual loss and blindness in the United States and worldwide. Specifically, we plan to determine
mechanisms of action and to measure preservation of neuronal viability and function in model
systems of glaucoma. The proposed research of the parent award will allow us to generate
preclinical data needed for the development of novel neuroprotectants to complement existing
therapies targeting intraocular pressure. The research proposed under the present Alzheimer's
disease (AD)-focused administrative supplement application will allow us to build on these novel
preclinical data sets and thereby to develop a novel therapeutic strategy for the protection of
neurons of the central nervous system (CNS) affected by AD. Specifically, we will test the
hypothesis that similar to neurons of the retina and optic nerve affected by glaucoma, the lack of
cellular defense mechanisms resulting from AD pathology reducing viability and function of CNS
neurons can be attenuated by the novel therapeutic strategy under development in the parent
award. To this end, a novel intervention approach will be developed that can be exploited to
devise novel treatments that can be delivered to CNS neurons affected by AD protecting them
from oxidative stress mediated damage and loss of function. Three-dimensional (3D) bio-printed
human neural cell constructs will be used as in vitro models for AD and for drug discovery in AD
and related dementias employing experimental strategies aligned with the parent award. The
proposed experiments will determine the potential of the targeted novel therapeutic strategy for
preventative and neuroprotective therapies in AD. The innovative strategy has the potential to
generate a first-in-class pharmacotherapy approach for AD. The strategy's potentially high
impact lies in its capacity to be both preventative and therapeutic in nature and to complement
current and future treatment designs and rationales.

## Key facts

- **NIH application ID:** 10288383
- **Project number:** 3R01EY031248-02S1
- **Recipient organization:** UNIVERSITY OF MISSOURI KANSAS CITY
- **Principal Investigator:** Peter Koulen
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $391,250
- **Award type:** 3
- **Project period:** 2020-02-01 → 2023-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10288383

## Citation

> US National Institutes of Health, RePORTER application 10288383, Novel mechanism controlling calcium signaling to treat and prevent neurodegeneration in early stage glaucoma (3R01EY031248-02S1). Retrieved via AI Analytics 2026-05-29 from https://api.ai-analytics.org/grant/nih/10288383. Licensed CC0.

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