A recent study published in Nature Communications suggests that an individual’s “bioenergetic age”—a measure of how efficiently their cells produce energy—could be a key predictor of Alzheimer’s disease risk. Conducted by researchers at Weill Cornell Medicine, this study offers hope that healthy living can not only turn back the bioenergetic clock for some individuals but may help fend off Alzheimer’s disease just as effectively as emerging drug treatments like lecanemab.
Understanding Bioenergetic Age and Alzheimer’s Disease Risk
Alzheimer’s disease is often preceded by early signs of brain cells losing their ability to produce and utilize energy efficiently, particularly in the metabolism of glucose. However, some individuals do not show symptoms of Alzheimer’s until many years after these energy dysfunctions begin. This delay suggests the existence of a “bioenergetic capacity”—a resilience that allows the brain to maintain normal energy levels despite the onset of cellular issues.
For some people, this higher bioenergetic capacity helps them maintain cognitive function into old age without the cognitive decline typically seen in aging individuals. But what if there were a way to identify those who possess this higher bioenergetic resilience and provide interventions for those without it?
The Role of Acylcarnitines in Predicting Alzheimer’s Risk
Dr. Jan Krumsiek, the senior author of the study and an associate professor at Weill Cornell Medicine, along with his colleagues, turned to a class of molecules known as acylcarnitines. These molecules are associated with the breakdown of fats and proteins to generate energy and have been linked to cognitive decline. The researchers sought to determine if acylcarnitine levels could serve as biomarkers for Alzheimer’s risk.
Using data from the large-scale Alzheimer’s Disease Neuroimaging Initiative (ADNI), the team identified patterns between acylcarnitine levels and the severity of Alzheimer’s disease. Their findings revealed that individuals with higher acylcarnitine levels had a higher “bioenergetic age” and experienced worsened Alzheimer’s pathology, cognitive decline, and brain atrophy. On the other hand, participants with lower acylcarnitine levels experienced slower cognitive decline.
Bioenergetic Age and Cognitive Decline
The researchers further quantified cognitive decline using the mini-mental state examination (MMSE), a commonly used test for assessing cognitive function. They found that people with lower acylcarnitine levels showed a slower rate of cognitive decline, losing about 0.5 fewer points per year on the MMSE compared to those with higher acylcarnitine levels. This benefit was similar to the effects observed with lecanemab, an Alzheimer’s drug that has garnered attention for its potential in slowing disease progression.
The study also found that bioenergetic age is influenced by both genetics and lifestyle. Genetics play a role in determining how quickly a person’s bioenergetic clock ticks forward. However, lifestyle factors such as a plant-based diet and regular physical activity can help lower acylcarnitine levels, keeping bioenergetic age younger.
Identifying Those Most at Risk
The study also identified a subgroup of individuals within the ADNI study—approximately 30% of participants—who had a higher bioenergetic age but also carried a favorable genetic background. These individuals may benefit more from early lifestyle interventions that aim to reduce their bioenergetic age, potentially delaying or even preventing the onset of Alzheimer’s disease.
Next Steps: Personalized Interventions for Lowering Bioenergetic Age
Dr. Krumsiek and his team plan to continue their research to determine which lifestyle interventions are most effective at lowering bioenergetic age. For instance, they are exploring how a low-carb diet might help maintain metabolic health, though they seek to identify how low carbohydrate consumption would need to be to produce benefits.
Additionally, the study highlights the potential for an inexpensive, rapid blood test to measure acylcarnitine levels, which could help assess a person’s bioenergetic age. This test, originally developed to identify metabolic and mitochondrial disorders in newborns, could be repurposed for use in older adults. Early identification of bioenergetic age through this test could pave the way for personalized treatments and interventions to reduce Alzheimer’s risk before symptoms appear.
Conclusion
This study marks a significant step toward understanding how bioenergetic age could serve as an early indicator of Alzheimer’s disease risk. By assessing acylcarnitine levels, it may soon be possible to identify individuals at risk and provide personalized lifestyle interventions to lower their bioenergetic age. These findings offer a promising approach to reducing Alzheimer’s risk and could potentially complement current treatments, offering a more holistic, preventive strategy for brain health.
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