# Genomics of Intracerebral Hemorrhage and its Causes

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA AT DAVIS · 2020 · $606,965

## Abstract

Abstract
 Following Intracerebral Hemorrhage (ICH), the blood–brain barrier (BBB) is disrupted with
associated edema and leukocyte extravasation from blood into the tissue/hematoma. Neutrophils,
monocytes and lymphocytes enter brain. Increased neutrophils or increased neutrophil to lymphocyte
ratio in humans are associated with worse ICH outcomes. Thus this proposal will examine gene
expression in neutrophils, monocytes and T lymphocytes following ICH as compared to ischemic stroke
and controls. ICH mortality is very high, with ICH volumes and edema volumes and causes of ICH being
important factors in survival. Thus, this proposal will examine gene expression in neutrophils, monocytes
and T lymphocytes as function of ICH volume, edema volume and ischemic lesion volume around ICH,
as well as causes of ICH. We expect different blood/ leukocyte/ platelet profiles for different ICH volumes
and different ICH causes that affect hematoma resolution, recurrent bleeding, and severity of recurrent
bleeding that would be molecular targets for improving survival. Based upon very robust preliminary data
we propose the following aims.
 Aim #1a. Demonstrate that proinflammatory genes are expressed at early times (12h, 1d, 3d) in
neutrophils, M1 monocytes and specific T cell subsets (γδT cells) following ICH; and immune-related
repair genes in M2 monocytes and specific T cell subsets (e.g. T helper cells) are expressed at later
times following ICH (3d, 7d); and, show the genes and pathways differ from those for ischemic stroke.
Aim #1b. Demonstrate specific T cell, and T-cell receptor gene expression decreases in blood following
ICH and this may correlate with decreased numbers of blood T lymphocytes (γδT early; T helper, Tregs
later). Aim #2. Determine the genes and pathways that correlate with volume of ICH, edema and
ischemic lesions around ICH over time, after accounting for differences in treatment for different sized
ICH. Aim #3a. Identify specific genes and pathways associated with deep ICH related to hypertension
compared to cortical lobar ICH related to probable CAA as defined by the modified Boston Criteria23-25.
Aim #3b. Demonstrate that, though there are some common genes and pathways associated with all
causes of ICH, there are large numbers of genes and pathways that are specific for each cause.
 The molecular underpinnings underlying human ICH are largely unexplored. Thus, this proposal
will begin to increase our understanding of human ICH by identifying molecules that correlate with factors
associated with ICH outcomes (neutrophils, monocytes, T lymphocytes, as well as ICH volumes and
edema volumes, and causes of ICH) that might be treatment targets to improve ICH outcomes.

## Key facts

- **NIH application ID:** 9898489
- **Project number:** 5R01NS106950-02
- **Recipient organization:** UNIVERSITY OF CALIFORNIA AT DAVIS
- **Principal Investigator:** Bradley Pearce Ander
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $606,965
- **Award type:** 5
- **Project period:** 2019-04-01 → 2024-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9898489

## Citation

> US National Institutes of Health, RePORTER application 9898489, Genomics of Intracerebral Hemorrhage and its Causes (5R01NS106950-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9898489. Licensed CC0.

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