# Neurochemical and inflammatory biomarkers of the trajectory of depressive symptoms after acute illness

> **NIH NIH R21** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2022 · $234,000

## Abstract

ABSTRACT
 Depressive symptoms frequently accompany acute illness and are associated with delayed recovery and
return to premorbid function, as well as increased healthcare costs. In illnesses such as acute ischemic stroke,
depressive symptoms and major depression occur in at least 30-50% of patients, yet little is known about the
evolution or mechanism of the symptoms. Our overall hypothesis is that early neurotransmitter and
inflammatory changes are biomarkers of subsequent depressive symptom trajectory. Understanding the
biomarkers and pathophysiology of depressive symptoms after acute stroke is crucial because it can guide
treatment to prevent symptoms from developing into an independent illness.
 In this project, we will identify multimodal biomarkers of depressive symptom trajectory after acute ischemic
stroke. Our biomarkers will include levels of neurometabolites (glutamate and GABA) and a cerebral
antioxidant (glutathione) as well as inflammation (both transcriptional and peripheral). Acute ischemic stroke is
a `high signal' environment as there are known changes in both neurometabolites and inflammation and a high
incidence of depressive symptoms.
 Our approach includes a novel advance over previous work through the simultaneous measures of multiple
neurometabolites/antioxidant and indices of the inflammation cascade. While previous work has demonstrated
relations between neurometabolites and inflammation in MDD, none of these factors have been examined
simultaneously as biomarkers of depressive symptom trajectory following acute stroke.
 We will enroll 40 participants with a range of depressive symptoms who have been admitted for an acute
initial ischemic stroke at the UCLA Comprehensive Stroke Center. At study entry, our carefully phenotyped
sample will receive: a magnetic resonance spectroscopy (MRS) scan, assays of peripheral and transcriptional
measures of inflammation; and measures of depressive symptoms. Inflammation measures will be repeated
after one month to explore early inflammatory change as a potential biomarker. For four months we will obtain
bimonthly ratings of depressive symptoms ratings and, for exploratory purposes, anxiety, quality of life, and
level of daily function.
 We hypothesize that initial levels of neurometabolites/antioxidant and inflammation will be related to early
depressive symptoms. Further, we hypothesize that neurometabolite and cerebral antioxidant levels, as well as
early changes in inflammation, will predict the depressive symptom trajectory. This information will provide
valuable insight into the pathobiology and course of depressive symptoms and create the foundation for future
larger-scale studies and potential interventions.

## Key facts

- **NIH application ID:** 10453402
- **Project number:** 1R21MH127520-01A1
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **Principal Investigator:** JOHN O BROOKS
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $234,000
- **Award type:** 1
- **Project period:** 2022-02-01 → 2024-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10453402

## Citation

> US National Institutes of Health, RePORTER application 10453402, Neurochemical and inflammatory biomarkers of the trajectory of depressive symptoms after acute illness (1R21MH127520-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10453402. Licensed CC0.

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