# Scrutinizing neuro-immune regulatory mechanisms underlying depressive symptomatology in young adults with HIV

> **NIH NIH R21** · UNIVERSITY OF CALIFORNIA, SAN DIEGO · 2022 · $237,000

## Abstract

Project Summary/Abstract
 Mood disorders are prevalent among individuals living with HIV for which multi-dimensional, contributing
factors exist. Especially, 20-50% of youth living with HIV (YWH) report depression or elevated depressive
symptoms of clinical relevance. Depression or elevated depressive symptoms in YWH result in HIV include
poor adherence to HIV treatment, poor viral suppression, increased morbidity and mortality as well as
decreased quality of life. In spite of growing data showing the association between blood inflammatory markers
and levels of depressive mood or clinical depression in HIV- and HIV+ individuals, inconsistent findings across
the studies in the inflammatory marker-depression associations pose challenges in understanding mechanisms
and lead to a paucity of targeted therapeutics. Given the profound modulatory effects of multiple branches of
the neuroendocrine system on immune/inflammatory activities, we propose to conduct simultaneous
investigations of potentially concurrent but disparate neuro-immune pathways (“NIP”) of inflammation
dysregulation (IR) in predicting depressive symptoms in 45 YWH and 45 Control youth (aged 18-25 yrs), by
leveraging an ongoing R01 study of brain function and cannabis use in YWH (DA047906). We will employ an
ex vivo cellular model of peripheral blood monocytes by which effects of various receptor agonists in cellular IR
will be assessed [1) sympatho-adrenal (SA)/adrenergic receptor (AR); 2) glucocorticoid (GC)/GC receptor
(GR), and 3) dopaminergic (DA)/DR pathways] in predicting depressive symptoms (Aim 1). The neuroimaging
markers of neuroinflammation from R01 [1) diffusion tensor imaging measures (e.g., fractional anisotropy), 2)
structural alterations (i.e., white matter abnormality), and 3) metabolites through MR Spectroscopy (i.e., higher
choline and myo-inositol, indicating diminished neuronal integrity and increased inflammation)] will be
examined as a mediator (Aim 2). We will also explore differing depressive symptom domains [1) cognitive, 2)
affective, and 3) somatic domains as well as 4) apathy and 5) anhedonia], as initial evidence shows symptoms
specific to HIV infection such as somatic symptoms and apathy which may provide insight into delineating NIP-
brain regions-symptoms network (Aim 3). Many types of the data collected in the R01 study will be shared with
this R21 such as sociodemographic; clinical; psychological and behavioral; and neuroimaging data, maximizing
the feasibility of this R21. Our simultaneous investigation of three NIP pathways with careful analytical plans in
predicting depressive symptoms will provide an opportunity to gain mechanistic knowledge beyond plasma
inflammatory marker-depression associations and to inform targeted therapeutic modalities.

## Key facts

- **NIH application ID:** 10487540
- **Project number:** 5R21MH128889-02
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN DIEGO
- **Principal Investigator:** Suzi Hong
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $237,000
- **Award type:** 5
- **Project period:** 2021-09-10 → 2024-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10487540

## Citation

> US National Institutes of Health, RePORTER application 10487540, Scrutinizing neuro-immune regulatory mechanisms underlying depressive symptomatology in young adults with HIV (5R21MH128889-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10487540. Licensed CC0.

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