What if one of the biggest clues to Alzheimer’s disease lies inside our mitochondria?
In this episode of Degrees of Health, Ben Hopkins is joined by Dr. Russell Swerdlow to explore the mitochondrial cascade hypothesis of Alzheimer’s — and why mitochondrial dysfunction could be playing a much bigger role in the disease than we once thought.
Russell talks through the research that led him to this hypothesis, including his early cybrid experiments, which found that mitochondrial DNA from Alzheimer’s patients could transfer reduced cytochrome oxidase activity into cell models. From there, the research uncovered a number of other changes, including increased oxidative stress, abnormal mitochondria, problems with calcium handling and changes in APP biology.
The conversation then gets into the metabolic side of Alzheimer’s. Why does the brain become less able to use glucose? What does “type 3 diabetes” actually mean? And why might mitochondrial dysfunction sit upstream of some of these changes?
They also discuss ketones, redox balance and the importance of keeping the brain’s “carbon rivers” flowing — and why targeting mitochondrial function could potentially be a more upstream approach than simply targeting amyloid plaques.
Russell also shares his thoughts on exercise, lifestyle and where future treatments could come from, including the possibility of using what we learn from lifestyle interventions to develop new pharmaceutical approaches.
And ultimately, there’s a much bigger question: could solving Alzheimer’s mean solving brain ageing itself?
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