UCL Division of Biosciences


Centre for Cardiovascular and Metabolic Neuroscience

Metabolic and cardiovascular disease are highly prevalent causes of morbidity and mortality in developed and ageing societies across the globe. The key role of disordered nervous control of metabolism and cardiovascular function is increasingly recognised in the pathogenesis of obesity, diabetes, and circulatory system disease. However, the mechanisms by which autonomic nervous system dysfunction contributes to the development and progression of these common conditions are not well understood.

To facilitate research in this area, the UCL Centre for Cardiovascular and Metabolic Neuroscience (CCMN) was established in 2014. Currently, CCMN brings together several UCL and external research groups that conduct basic and clinical studies directed at understanding the role of neural mechanisms in the development of cardiovascular, cerebrovascular, and metabolic disease.

Current Research

Brain energy metabolism and regulation of cerebral blood flow

The high metabolic rate of the brain, associated with the activities of billions of nerve cells processing information, requires constant and optimal nutrient and oxygen supply, as well as effective elimination of metabolic waste products, ensured by elaborate physiological mechanisms controlling cerebral blood flow. Sustained efficacy of these mechanisms maintains neurologic health and promotes brain longevity. There is growing evidence that reduction in the blood flow to the brain, resulting in impaired delivery of metabolic substrates, damages nerve cells and the connections between them, leading to cognitive decline, and the development of neurodegenerative disease, such as Alzheimer’s disease.

We study the fundamental biological processes that ensure nutritional support of nerve cell activity, effective elimination of CO2 as a major brain waste product, and the mechanisms activated in conditions of metabolic emergency, such as when oxygen supply to the brain is reduced. We investigate how brain blood flow is fine-tuned to support dynamic changes in local neuronal circuit activity and how brain blood flow is controlled to protect neuronal networks from deleterious changes in carbon dioxide concentration and oxygen availability.

This research is supported by The Wellcome Trust

Autonomic Dysfunction in Diabetes

Diabetes and its co-morbidities such as cardiovascular disease seriously impact on quality of life. Additionally, 10% of the NHS budget is spent on treatment of diabetes alone. Despite the epidemic scale of the problem, clinicians still lack reliable predictors, that help diagnose co-morbidities early, that serve as benchmarks for treatment success, and that determine individual patients' prognosis.

We hypothesize that changes in the autonomic nervous system, leading to imbalances between sympathetic and parasympathetic drives, promote the development of diabetes and related morbidities. The aim of this research is to develop a pre-clinical model of autonomic imbalance that allows us to systemically investigate its potential deleterious consequences.

The role of Glucagon-Like Peptide-1 in the control of energy homeostasis

GLP-1 receptor agonists have recently been shown to be the most efficacious anti-obesity drug to date. However, much of the physiology of GLP-1 remains unclear. GLP-1 is released from the gut into the bloodstream postprandially, but it is also produced by neurons located in the brainstem. Thus GLP-1 acts both as a hormone and as a neurotransmitter. Our work aims at delineating the effects of neuronal GLP-1 from those of gut-released GLP-1, in order to better understand its role in normal feeding behaviour, as well as in obesity and metabolic disease states.


We have recently demonstrated that activation of GLP-1 producing neurons elicits a reduction of food intake beyond that achieved with concomitant administration of a best-in-class GLP-1 receptor agonist highlighting the potential opportunities of combination therapy for the treatment of obesity. This research is primarily supported by the MRC and EFSD.

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Autonomic control of the heart during exercise

The brain controls the heart function by sending commands through specialised nerves. These brain-heart connections are vital to produce rapid changes in heart rate and determine how hard the heart works, which is essential for exercise, for example. Efficacy of communication between the brain and the heart increases as a result of exercise training and contributes to optimizing the exercise performance. In contrast, during the development of cardiovascular disease, diabetes, as well as in normal aging the activities of these nerves decline. This impairs communication between the brain and the heart rendering the heart unable to rapidly respond to changes in behavioural/physical demands and limiting our ability to exercise.


Our studies aim to determine the physiological principles underlying adaptive and maladaptive alterations in the efficacy of communication between the brain and the heart that develop in response to exercise training and during the progression of cardiovascular disease. Since maintaining physical activity is essential for every aspect of physical, emotional and cognitive health, we also aim to identify how these nervous mechanisms can be switched on to enhance the ability to exercise, increase quality of life and promote cardiovascular health across the lifespan.

This research is supported by The British Heart Foundation.

Gut-brain neural circuit dysfunction in obesity

Much of the global population now live in an obesogenic environment, characterised by ready availability of the ultra-processed, high-fat and high-sugar foods which comprise the modern 'Western diet'. This diet is a deleteriously effective trigger of the evolutionarily conserved drive to maximise energy intake during periods of food abundance. While susceptibility to the obesogenic environment is highly variable between individuals, at the population level it drives the chronic overconsumption of food now considered the primary cause of the obesity epidemic. Overconsumption can be caused by impaired function in the neurobiologically-distinct processes of satiety and/or satiation. Satiation processes ultimately elicit meal termination via a poorly understood interaction of neuronal and hormonal signalling pathways between the gastrointestinal tract and the brain - the so-called 'gut-brain axis'.

To prevent the development of obesity in susceptible individuals, and to help people living with obesity to decrease and sustainably maintain their weight, it is vital to understand why dysfunction occurs in the gut-brain pathways controlling meal termination, and how it can be prevented and/or reversed. However, the precise mechanisms underlying the function and dysfunction of these gut-brain satiation circuits are largely unknown. We use transgenic mouse models and systems neuroscience techniques including optogenetics / chemogenetics, electrophysiology, calcium imaging, transcriptomics and lipidomics to interrogate how gut-brain neurocircuits orchestrate meal termination at the cellular, molecular and behavioural levels.

This research is supported by The Wellcome Trust and The Royal Society.










Find out more about the history of Neuroscience research at UCL