# Pathway maps of platelet phenotype and function

> **NIH NIH R01** · OREGON HEALTH & SCIENCE UNIVERSITY · 2021 · $376,567

## Abstract

ABSTRACT FOR ADMINISTRATIVE SUPPLEMENT
Platelets are specialized peripheral blood cells that rapidly engage and resolve endothelial injury through
adhesion, secretion and aggregation responses. These regulated changes in platelet form and function are
essential to hemostasis and vascular health, but also support acute and chronic pathologies of aging (i.e.,
thrombosis, atherosclerosis).Translational efforts aiming to determine disease-specific platelet activities have
identified heterogeneous platelet phenotypes in the laboratory as well as in the clinic associated with acute
thrombotic and chronic inflammatory conditions – including vascular pathologies in Alzheimer’s disease and
related dementias (AD/ADRD). The mechanisms by which maladaptive platelet phenotypes arise in disease
are unclear. Efforts to develop effective therapeutic, diagnostic and preventive strategies focused on
maladaptive platelets in aging and vascular diseases remain to be actualized. In this Administrative
Supplement, we aim to determine how Alzheimer’s disease etiology relates to alterations in molecular
programs of platelets that support inflammatory and thrombotic responses associated with disease. Our central
hypothesis is that signaling systems underlying platelet cell physiological responses are specifically
dysregulated in Alzheimer’s disease in a manner promoting as well as marking disease progression. As a
supplement to our parent award, this study will make further use of a high-throughput, proteomics-based
workflow to measure and map intracellular signaling events in platelets isolated from donors with Alzheimer’s
disease relative to platelets from age and sex matched mild cognitive impairment (MCI) and normal cognition
(NC) control donors. In collaboration with clinicians and researchers from the NIA P30-supported Oregon
Alzheimer’s Disease Center (OADC), our multidisciplinary team will systematically define how Alzheimer’s
disease relates to alterations in intracellular signaling events that orchestrate platelet adhesion (Aim 1),
secretion (Aim 2) and aggregation (Aim 3) in the context of vascular inflammation and Alzheimer’s disease
progression. As a major goal of the parent award is to determine how maladaptive platelet phenotypes
develop, and, ultimately, how they may be targeted and managed, this Supplement provides a unique
opportunity to add value to ongoing studies while advancing Alzheimer’s disease research with state-of-the-art
methods. Ultimately, this work will generate knowledge as well as a conceptual means to understand how to
better predict, detect and manage Alzheimer’s disease.

## Key facts

- **NIH application ID:** 10284852
- **Project number:** 3R01HL146549-03S1
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** Joseph E Aslan
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $376,567
- **Award type:** 3
- **Project period:** 2019-04-01 → 2024-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10284852

## Citation

> US National Institutes of Health, RePORTER application 10284852, Pathway maps of platelet phenotype and function (3R01HL146549-03S1). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10284852. Licensed CC0.

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