• 2018-present, UK Dementia Research Institute Fellow & Senior Lecturer, University of Edinburgh

• 2014-2018, Group Leader, The Roslin Institute, University of Edinburgh
• 2010-2014, Career-track fellow, The Roslin Institute, University of Edinburgh
• 2008-2010, Postdoctoral research associate, University of Manchester (Kell/Rothwell labs)
• 2004-2008, Postdoctoral research associate, University of Manchester (Rothwell/Allan labs)

2000 BSc (Hons) Neuroscience, University of Glasgow

2004 PhD University of Glasgow

https://www.ed.ac.uk/discovery-brain-sciences/our-staff/research-groups/dr-barry-mccoll

https://ukdri.ac.uk/team/barry-mccoll

The overall goal of our research is to understand neuroimmune mechanisms influencing brain injury, repair and disease in order to identify new targets for treatments

The overall goal of our research is to understand neuroimmune mechanisms influencing brain injury, repair and disease in order to identify new targets for treatments. We have particular interests in cerebrovascular disease (stroke and vascular cognitive disorders) and neurodegenerative diseases linked to dysfunction of microglia and neuroimmune regulation. Research in the lab largely encompasses three major strands each of which involves a range of molecular, cellular and organismal approaches using preclinical models, human samples and patient-based investigation.

Key research themes:

• Microglial mechanisms of resilience and susceptibility to neurodegenerative disease
• Role of myeloid cells in brain injury and repair
• Neuroimmune signalling and systemic immune dysfunction after stroke

The overall goal of our research is to understand neuroimmune mechanisms influencing brain injury, repair and disease in order to identify new targets for treatments. We have particular interests in cerebrovascular disease (stroke and vascular cognitive disorders) and neurodegenerative diseases linked to dysfunction of microglia and neuroimmune regulation. Research in the lab largely encompasses three major strands each of which involves a range of molecular, cellular and organismal approaches using preclinical models, human samples and patient-based investigation.

Microglial mechanisms of resilience and susceptibility to neurodegenerative disease

Microglia are the specialised brain resident macrophages with important developmental, physiological and neuroinflammatory functions. Their dysfunction is increasingly implicated in neurodegenerative diseases leading to dementia. Work in our lab has contributed to the growing recognition of considerable diversity in microglial phenotypes in the healthy, ageing and diseased brain. This diversity may predispose to susceptibility or resilience to disease and influence the course of disease in space and time in distinct ways. The discovery of dementia-causing neurodegenerative diseases where mutations in microglial-expressed genes appear causal or increase risk and which show distinctive vulnerability in specific neuroanatomical compartments (particularly white matter), supports a disease-modifying role for microglia in disease. Our work is using models of neurodegenerative disease and human tissue to explore mechanisms that regulate microglial phenotype, how phenotypic diversity confers resilience and susceptibility to disease, and to identify potential therapeutic targets directed at manipulating or restoring microglial function.

Myeloid cells in brain injury and repair

Myeloid cells are the key orchestrators of innate immune responses and inflammation. As in other tissues, inflammation can have harmful effects in the brain that can aggravate injury but some forms of activity by certain subsets of inflammatory cells is important to enable injured brain tissue to heal and promote recovery of function. Our research is examining regulatory factors that control the subtypes of myeloid cells that accumulate in the injured brain (e.g. after ischaemic and haemorrhagic stroke) and their diverse activation states which we believe is crucial to understand the balance between harmful and helpful inflammation and to identify pro-repair/regenerative phenotypes. Using preclinical models, we are also testing the effects of myeloid cell-targeted compounds to manipulate these cells towards tissue repair phenotypes.              

Neuroimmune signalling and systemic immune dysfunction after stroke

Stroke is a leading cause of death and disability and in addition to the brain damage itself, complicating factors have an important bearing on outcome and functional recovery. Pneumonia is common after stroke and is one of the most important stroke complications associated with poor outcome. Our work has contributed to the increasing recognition that stroke can cause suppression of certain aspects of systemic immune function that normally protects us from infection. These changes may partly explain the high risk of pneumonia and other infections in stroke patients and could offer new approaches for prevention. In particular, we study how B cell function may be impaired after stroke including dysfunction of certain subtypes of B cells with innate-like functions providing protection early after infection. Neural signalling, such as via the sympathetic nerves, appears important in driving dysfunction of B cells and other immune cells after stroke and our ongoing work is investigating this brain-to-immune signalling in more detail. We are also investigating if treatments that could rescue B cell function (or compensate for their impairments) could be beneficial in preventing stroke-associated infection.  

Current PhD students

Clare Latta

Anirudh Patir

Caoimhe Kirby

James Loan

Makis Tzioras

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, sucha s infection, outside the brain can affect the recovery from brain injury.

Associate Editor, BMC Neuroscience

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