A study conducted by UCL scientists has uncovered a crucial mechanism that identifies when the brain requires an extra energy boost to sustain its functions.
The study published in Nature reveals findings that could guide the development of new treatments to support brain health and longevity. Previous research has indicated that impaired brain energy metabolism in late life can lead to cognitive decline and neurodegenerative diseases.
Lead researcher Professor Alexander Gourine from UCL Neuroscience, Physiology & Pharmacology, explained that the brain, composed of billions of nerve cells, relies on a continuous supply of nutrients and oxygen due to its energy-demanding nature, especially during challenging tasks like movement control, learning, and memory formation.
It has been established that a type of glial cell called astrocytes assist neurons in obtaining the required energy. When nearby neurons require an energy increase, astrocytes act swiftly by activating their glucose stores and metabolism, resulting in the production and release of lactate, which serves as an additional energy source for neurons.
Through their research, the team discovered how astrocytes monitor the energy consumption of neighboring nerve cells and initiate the delivery of additional energy to active brain regions.
Experiments with mouse models and cell samples identified specific receptors in astrocytes that detect neuronal activity and activate a signalling pathway involving adenosine, a crucial molecule. The pathway activated by adenosine in astrocytes is akin to the one found in muscles and the liver during exercise, facilitating energy supply to neurons for uninterrupted synaptic function.
Activating astrocyte glucose metabolism via adenosine ensures that synaptic function proceeds smoothly during periods of high energy demand or reduced energy supply.
Deactivating the key astrocyte receptors in mice led to impaired brain activity, affecting brain metabolism, memory, and sleep. This highlights the significance of the identified signalling pathway in processes like learning and memory.
Dr. Shefeeq Theparambil, the study’s first author, highlighted the broader implications of identifying this mechanism, suggesting it could be a potential approach in treating brain disorders associated with compromised brain energy, such as neurodegeneration and dementia.
Professor Gourine emphasized that as brain energy regulation deteriorates with age, and particularly in neurodegenerative diseases like Alzheimer’s, their study presents a promising target for intervention to safeguard brain function, cognitive health, and longevity.
The research, supported by Wellcome, involved collaboration among scientists from several institutions including UCL, Lancaster University, Imperial College London, King’s College London, Queen Mary University of London, University of Bristol, University of Warwick, and University of Colorado.
