Dr. Mark Mattson, National Institute on Aging and Johns Hopkins University
Maintaining optimal brain function throughout life requires effort
Humans evolved in environments where food was not available ad libitum, and so possess robust adaptive physiological and behavioral responses to periods of food scarcity. Emerging research in this Laboratory and elsewhere has shown that intermittent fasting (IF; for example, fasting for a period of 24 hours twice weekly) and vigorous exercise can increase numbers and strength of synapses and can enhance brain function (cognitive and sensory – motor performance) and mood. Our studies in animal models of chronic neurodegenerative disorders (Alzheimer’s and Parkinson’s diseases) and acute brain injury (stroke and severe epileptic seizures) demonstrate robust neuroprotective and neurorestorative effects of IF diets. The general mechanism by which IF and exercise benefit neurons is by increasing their activation state and energy demand, which results in a coordinated series of responses that promote neuroplasticity and cellular stress resistance. The pathways activated by exercise and IF include those involving brain-derived neurotrophic factor (BDNF), mitochondrial biogenesis, DNA repair and removal of oxidatively damaged proteins and organelles (autophagy). Peripheral changes in energy metabolism that occur during fasting and exercise may also contribute to their beneficial effects on the brain. In this regard, the depletion of glycogen stores in the liver triggers the mobilization of fatty acids from fat cells and the production of ketone bodies. Ketone bodies such as beta-hydroxybutyrate provide an alternative energy source for neurons and may also activate signaling pathways that enhance the ability of the brain to cope with stress. Finally, emerging findings suggest that some of the chemicals in fruits and vegetables that may improve brain health do so by activating adaptive cellular stress responses; from an evolutionary perspective the phytochemicals function as toxic agents/antifeedants. The implications of these findings for strategies for optimizing brain function and reducing the risk of neurodegenerative disorders will be described.
Dr. Mark Mattson is currently Chief of the Laboratory of Neurosciences at the National Institute on Aging, and Professor of Neuroscience at Johns Hopkins University. He is Editor-in-Chief of Ageing Research Reviews and NeuroMolecular Medicine, a Section Editor for Neurobiology of Aging, and an Associate Editor for Trends in Neurosciences. In addition, he has edited 10 volumes in the areas of mechanisms of brain function, stress responses, aging and age-related neurodegenerative disorders. Dr. Mattson is a Fellow of the American Association for the Advancement of Science, and has received numerous awards including the Metropolitan Life Foundation Medical Research Award and the Alzheimer’s Association Zenith Award. He is considered a leader in the area of cellular and molecular mechanisms underlying neuronal plasticity and neurodegenerative disorders, and has made major contributions to understanding of the pathogenesis of Alzheimer’s disease, and to its prevention and treatment. Dr. Mattson has published more than 400 original research articles and more than 200 review articles and commentaries.
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