Ignite Creation Date:
2024-05-06 @ 8:08 PM
Last Modification Date:
2024-10-26 @ 3:21 PM
Study NCT ID:
NCT06263452
Status:
RECRUITING
Last Update Posted:
2024-05-09
First Post:
2024-01-31
Brief Title:
Beta-Blocker Influences on Inflammatory and Neural Responses to Stress
Sponsor:
University of North Carolina Chapel Hill
Organization:
University of North Carolina Chapel Hill
Study Overview
Official Title:
Beta-Blocker Influences on Inflammatory and Neural Responses to Stress
Status:
RECRUITING
Status Verified Date:
2024-05
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
The purpose of this study is to map the neural and molecular mechanisms underlying psychological stress-induced changes in inflammation which could reveal new targets for intervention to reduce the risk of cardiovascular disease
Detailed Description:
The proposed work will conduct a mechanistic clinical trial utilizing the non-selective beta-adrenergic receptor blocker propranolol to examine the role of beta-adrenergic signaling in shaping neural and inflammatory responses to stress The investigators will focus on beta-adrenergic signaling given seminal pre-clinical work showing that this molecular pathway is an important driver of stress-related increases in inflammation and initial human neuroimaging work showing that beta-blockade leads to changes in neural responses to negative stimuli Here the investigators will bring these two previously disparate lines of work together to determine how experimentally blocking one critical stress-signaling pathway shapes neural activity and inflammatory responses to stress In doing so the investigators will be advancing knowledge by mapping mechanisms ie beta-adrenergic signaling offering methodological improvements ie moving beyond correlation to using pharmacological manipulations to provide causal evidence and identifying intervention targets ie the neurocognitive systems that shift activityconnectivity in response to beta-blockade In sum the work proposed herein is significant because it will address the mechanisms by which one critical risk factor psychological stress may ultimately lead to cardiovascular disease via inflammation The proposed study also offers significant methodological improvements over past work by using neuroimaging to identify neurocognitive pathways and pharmacology to provide causal experimental evidence to move us beyond correlation Finally this project is significant because it could provide insight into novel targets for future interventions
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
True
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
False
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| 1R01HL157422-01 | NIH | None | httpsreporternihgovquickSearch1R01HL157422-01 |