Edinburgh Research Explorer

Dr Barry McColl

Senior Research Fellow

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Willingness to take PhD students: Yes

Education/Academic qualification

2004Doctor of Philosophy (PhD), University of Glasgow
2000Bachelor of Science, University of Glasgow

Area of Expertise

Research expertiseNeuroimmune biology, Inflammation, Stroke, Microglia


I graduated from the University of Glasgow with a BSc (Hons) Neuroscience and then began my research training at the Division of Clinical Neuroscience, University of Glasgow, where I completed my PhD under the supervision of Prof Karen Horsburgh. During my PhD I studied the influence of polymorphism in the APOE gene on neuronal injury and the mechanisms underlying differential responses to cerebral ischaemia. A key finding was that APOE polymorphism influences neuronal and glial endocytic function in the injured human brain.

I moved to the University of Manchester to undertake postdoctoral studies in the lab of Prof Nancy Rothwell and Prof Stuart Allan. Here I investigated the impact that inflammation arising outside the brain (e.g. infection) has on the inflammatory and pathological responses to acute cerebral ischaemia. Key discoveries were the involvement of changes to the blood-brain barrier and amplified innate immune responses in the exacerbation of brain damage caused by systemic inflammation. Other findings included the deleterious effect of obesity on experimental stroke, mechanisms of neutrophil-mediated neurotoxicity and the involvement of platelets in cerebrovascular inflammation. I continued postdoctoral work at the University of Manchester (under Prof Doug Kell, Prof Nancy Rothwell) on a project using computational approaches to identify effective novel anti-inflammatory agents.  Key findings were that that an evolutionary algorithm can efficiently find effective combinations of anti-inflammatory drugs from a vast chemical library and that multi-component drugs out-perform single agents.

I then moved to The Roslin Institute, University of Edinburgh to establish my own research group in the Division of Neurobiology. The major aims of my group’s work are to understand how neuroimmune interactions contribute to normal brain homeostasis and how the immune system influences acute and chronic neurodegeneration.



2000 BSc (Hons) Neuroscience, University of Glasgow

2004 PhD University of Glasgow


Current Research Interests

Major aims of our research are to understand how neuroimmune interactions contribute to normal brain health and how the immune system influences neurodegeneration, regeneration. and complications of brain injury.

Research Interests

Our research is broadly divided into two major inter-related themes:

(i) understanding how interactions between the brain and immune cells help regulate normal brain function

(ii) understanding how immune and inflammatory processes contribute to chronic neurodegeneration and acute brain damage, repair and complications

Our overall aim is to use this understanding to develop new approaches for preserving healthy brain function, preventing or minimising neurodegeneration and promoting repair and recovery after brain injury in patients

1. Microglial phenotypic diversity

Bi-directional communication between the CNS and immune system occurs at several spatial scales and is essential for normal function of both systems. At the cellular level within the brain, microglia (the resident macrophages of the CNS) communicate with all other cell types including neurons. We are studying the transcriptional basis for regional microglial diversity that enables them to adapt to their microenvironment and support neuronal function. We are also interested in how ageing affects microglial transcriptional profiles, their regional diversity and the impact of co-existing systemic inflammation.

2. Immune and inflammatory mechanisms of neurodegeneration

Innate and adaptive immune responses are essential for host defence against infection and tissue repair but inappropriate, excessive or mis-directed inflammatory and immune processes can also cause or exacerbate tissue damage and dysfunction. Extensive evidence implicates inflammation as a pathological mechanism in a range of acute brain injuries (hypoxia, ischaemia, trauma) and chronic neurodegenerative conditions (e.g. Alzheimer’s Disease, Parkinson’s Disease). We aim to understand molecular and cellular inflammatory mechanisms that contribute to acute brain injury and promote neurodegeneration and identify potential therapeutic targets.

3. Resolving inflammation and the balance between injury and repair in the brain after stroke

Stroke causes one in ten of all deaths worldwide and is the leading cause of adult neurological disability. Understanding what influences the transition and balance between injury and repair in the post-ischaemic brain is recognised as one of the most important challenges in the field (e.g. has been referred to as the “new penumbra”). In this context, establishing how pro-injurious inflammation can be contained or resolved without compromising the capacity for endogenous or exogenously-triggered brain repair is essential. We are studying the mechanisms that regulate this balance with a particular focus on the function of the TREM2 protein and interactions among myeloid cell populations in the brain.

4. Stroke-induced immunosuppression

Infection is the most common complication affecting stroke patients and the leading cause of death after the brain injury itself. The reasons for this susceptibility are unclear but may involve suppression of some immune functions involved in host defence to bacterial infection. Our work is investigating how stroke-induced changes in the immune capabilities of lymphoid tissues such as the spleen, notably their ability to capture and process antigen and mount effector responses, may predispose to infection.


Research students



Stefan Szymkowiak

Clare Latta

Anirudh Patir

Alejandra Sanchez Quintero


Rebecca Madden

Dina Bugyabayeva




Stephen Booth

Kathleen Grabert

Claire Davies

Mari Pattison


Simao Wu 

Mubashra Shahid



Rosie Owens

Alicia Garcia

My research in a nutshell

The central nervous system and immune system engage in many interactions that keep us healthy and prevent the brain from degenerating. We study some of these interactions and try to identify how they work and how they might be augmented to reduce ageing-related impairments in brain function. Sometimes, inappropriate or excessive activation of the immune system can also cause tissue damage in the brain, for example after an injury like a stroke. We investigate how this occurs and how to dampen the immune response to minimise damage and promote repair in the injured brain. We also study how immune complications outisde the brain can affect the recovery from brain injury.

Administrative Roles

Associate Editor, BMC Neuroscience

Member, Young Investigator Committee, International Society for Cerebral Blood Flow & Metabolism

Research activities & awards

  1. Neuroimmune regulation and relevance to neurodegeneration

    Activity: Academic talk or presentation typesInvited talk

  2. British Neuroscience Association 2015: Festival of Neuroscience

    Activity: Participating in or organising an event typesParticipation in conference

  3. Neuroimmune interactions in CNS health, degeneration and repair

    Activity: Participating in or organising an event typesParticipation in conference

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