Dietary energy substrates reverse early neuronal hyperactivity in a mouse model of Alzheimer's disease

What is it about?

We show that the Alzheimer’s disease (AD)-related epilepsy (Alzheimer patients are 87 times more likely to develop epilepsy) is caused by a toxic substance (beta-amyloid) that is overproduced in AD brains, and that beta-amyloid causes this epilepsy by directly interfering with how brain cells use energy (in form of glucose), resulting in energy starvation of the neurons. When that happens, neurons become overexcited and unable to properly function. We also show that this beta-amyloid toxicity could be prevented by providing alternative energy fuels (such as pyruvate, completely safe and available over-the-counter in any health nutrition stores).

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Why is it important?

We are the first to directly link AD-related epilepsy to beta-amyloid toxicity on energy metabolism; Until now, beta-amyloid was thought to modify nerve cells' basic electrical function parameters by directly and mechanistically interfering. However, we now show that this effect is mainly through induced energy deprivation. Most importantly, we show that this effect could be completely blocked by chronic dietary supplementation with pyruvate.