Inflammatory Mediators of Cerebral Autoregulation in Acute Brain Injury

Summary

Clinical treatments of acute brain injury (ABI) are currently targeted at the brain injury processes that happen after the initial brain damage, such as the loss of cerebral autoregulation (CA). CA is the brain’s mechanism of maintaining adequate blood flow over a range of blood pressures, and this mechanism is known to fail/function sub-optimally in many patients suffering from ABI. However, we do not fully understand how this mechanism works, and therefore we cannot avoid its failure in these patients.  

Project aims

This project aims to explore the role of vascular and endothelial inflammation in CA and cerebral blood flow control. Previous work has identified the complement cascade as a key pathway in linking vascular inflammation and intracranial physiology post brain injury. This project will follow on from this work and will include both wet lab aspects (human biological sample collection, and analysis via single and multiplexing protein assays), as well as computational data analysis of high frequency physiological data. This project would suit individuals with laboratory experience, as well as considerable data handling, analytical, and computational skills. 

Contact details

Mr Adel Helmy, aeh33@cam.ac.uk – Neurosurgery

Supervised by Mr Adel Helmy and Dr Peter Smielewski.