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Recent Reviews Read, F1000 Factor: 8

Disrupted energy metabolism and neuronal circuit dysfunction in cognitive impairment and Alzheimer's disease. Kapogiannis D, Mattson MP. Lancet Neurol. 2011 Feb; 10(2):187-98

Evaluated by | Frank Nelson and Kevin Conley, University of Washington, United States of America


Food for thought: brain energy metabolism is key to neuronal cell function and cognitive health. 

A new hypothesis proposes a fundamental link between brain energetics and neural network function. This hypothesis is prompted by research findings that reveal that the state of energy metabolism adaptively modifies neuronal and brain networks. In maladies such as Alzheimer’s disease and aging, a decline in cognitive function is paralleled by changes in neuronal metabolism. Both animal and human studies reveal mitochondrial dysfunction and elevation of oxidative stress are a part of the decline in brain metabolism. These parallel changes in brain function and metabolism could occur as independent consequences of disease pathology. However, a second set of findings point to a link between these processes by demonstrating cognitive improvements after lifestyle alterations known to improve energy metabolism. Underlying this effect is the activation of adaptive responses, such as the cell stress response. This response has been found to elevate synaptic and neurogenic plasticity via neurotrophic factors (e.g. brain-derived neurotrophic factor [BDNF]). These factors also result in neuroprotection, reduction in oxidative stress and activation of neurogenesis. Thus, preservation of the integrity of existing neurons and facilitation of the genesis of new tissue could underlie the improvement of cognitive function found with chronic exercise or improvement in diet. This fundamental link between energetics and cognition provides a new interpretation of the phrase “food for thought”; perhaps the way to improve a brain’s function is through its energy metabolism.

Evaluated 25 May 2011