Analysis of HMGB1 and cell populations in injured brain tissue V1.0
Research type
Research Study
Full title
Analysis of the neuroinflammatory mediator HMGB1 and its impact upon cell populations in brain tissue following neurotrauma
IRAS ID
274166
Contact name
Ron Ved
Contact email
Sponsor organisation
Cardiff University
Clinicaltrials.gov Identifier
N/A, N/A
Duration of Study in the UK
1 years, 0 months, 7 days
Research summary
This MRC approved PhD studentship research project investigates the effect Traumatic Brain Injury (TBI) upon brain tissue. TBI is the most common cause of death and disability in young people. TBI can lead to unemployment and homelessness, family breakdown, resulting in a significant economic cost to the community. A critical challenge is to identify the mechanisms involved in brain tissue injury, death and repair, in order to identify potential new therapeutic targets to improve patient outcomes. Animal models of TBI have identified candidate substances that contribute to brain tissue injury. However, thus far, pharmacological interventions to modulate the impact of trauma upon brain tissue have not proved effective or practical. Understanding how neurotrauma affects human brain tissue in vitro is therefore a critical gap in the TBI literature which requires addressing.
A proportion of patients who suffer a TBI require neurosurgical evacuation of injured brain tissue (contusionectomy). This tissue is then discarded in clinical waste facilities and is of no further use to clinical practise. However, analysis of the cell components and mediators within this tissue may provide vital insights to the unmet clinical need to identify the mechanisms underlying brain damage caused by TBI in humans.
Our recent work has identified neuroinflammatory mediators, such as High Mobility Group Box Protein 1 (HMGB1) as impacting upon cell survival and repair in our and others’ animal data. There is thus an unmet research need to assess whether inflammatory mediators of neuroinflammation in human tissue. If this is confirmed, then neuroinflammatory mediators such as HMGB1 and its downstream pathways, could become strong candidates as a potentially modifiable mediators of brain damage after human TBI.
This study is part of an MRC grant-funded PhD studentship (Clinical Research Training Fellowship), covering consumables and supporting the development of the research throughout the studentship and beyond.REC name
Wales REC 7
REC reference
24/WA/0094
Date of REC Opinion
30 Mar 2024
REC opinion
Favourable Opinion