summary: Researchers have found that a person’s “bioenergy age” is strongly predicted, reflecting how efficiently cells generate energy to produce energy. A molecule at high blood cell levels, called acylcarnitine, a marker of aging metabolism, was associated with faster cognitive decline and greater Alzheimer’s disease symptoms.
However, lifestyle choices such as plant-based diets and regular exercise can effectively reduce these molecules, reduce bioenergy age, and delay the onset of Alzheimer’s disease. This bioenergy approach helps to identify at-risk individuals early and provide personalized strategies to maintain brain health without relying solely on drugs.
Important facts:
- Bioenergy Clock: High acylcarnitine levels indicate older bioenergy ages, which are significantly associated with the risk of Alzheimer’s disease.
- Lifestyle Benefits: A healthy lifestyle, including diet and exercise, can reduce bioenergy age and may provide protective benefits similar to Alzheimer’s disease.
- Personalized Prevention: Approximately 30% of study participants at genetic risk may benefit from lifestyle interventions, particularly those with a life style intervention.
sauce: Weil Cornell University
A new study from Weill Cornell Medicine can show that a person’s “bioenergy age” or is an important indicator of how young their cells produce energy.
This study was published on February 24th. Natural CommunicationIt suggests that a healthy lifestyle can turn back the bioenergy clock in some people, helping to dodge Alzheimer’s disease as effectively as a new drug called lecanemab.
“Weill Cornell Medicine’s Institute of Computational Biomedical Sciences and Computational Genomics,” said Jan Krumsiek, Ph.D., associate professor of physiology, biophysics and computational genomics at Weill Cornell Medicine’s Institute of Computational Biomedical Sciences. The first author of this study, Dr. Matthias Arnold, is head of Helmholtz Munich’s Computational Neurobiology Team.
The new findings bring us one step closer to solving a long-standing puzzle. One early warning sign of Alzheimer’s disease is that brain cells begin to lose their ability to efficiently generate and use energy efficiencies such as glucose (sugar). However, some people have not been showing symptoms of the disease for years.
This delay between abnormalities in the energy pathway and the onset of symptomatic diseases suggests that there is a “bioenergy ability” to provide buffers to these individuals. Their bodies and brains are excellent at raising energy levels even when problems start.
“In these cases, people can become abnormally healthy when they see cognition,” said Dr. Kurmiek, who is also a member of the Institute for English for Precision Medicine. “They make it in the old age without the decline that usually creeps up.”
But can researchers identify individuals with this beneficial bioenergy ability and help people without it?
A new tool to predict the risk of Alzheimer’s disease
Dr. Krumsiek and his colleagues turned to a group of molecules called acylcarnitines. This is related to cognitive decline, breakdown or metabolism of energy fats and proteins.
To test whether high acylcarnitine levels in the blood could predict who is at risk of developing Alzheimer’s disease, the researchers used data from a large study called the Alzheimer’s Disease Neuroimaging Initiative.
“It was fascinating,” Dr. Kurmiek said.
“Splitting study participants into groups based on specific acylcarnitine levels highlighted those with more severe Alzheimer’s disease and fewer symptoms.”
This led researchers to define bioenergy clocks based on acylcarnitine. This is how old a person’s metabolism is compared to their actual age. Higher bioenergy age is associated with higher acylcarnitine levels, and is associated with worsening Alzheimer’s disease, cognitive decline, and brain atrophy.
Researchers also quantified cognitive decline using a general test called mini-mental status tests. A score of less than 24 out of 30 points indicates a disability.
They found that people starting with people with low acylcarnitine levels decrease more slowly, and about 0.5 percentage points per year less than people with high acylcarnitine levels. Its advantage is comparable to the Alzheimer’s drug lecanemab.
To some extent, a human bioenergy clock will tick forward at a speed determined by genetics, but having a healthy lifestyle of eating and exercising, for example, a plant-based diet can help keep acylcarnitine levels low.
They continued to identify subgroups of participants, which are approximately 30% of the neuroimaging initiative for Alzheimer’s disease.
These individuals may benefit more from early lifestyle interventions designed to reduce bioenergy age and potentially prevent the onset or prevention of Alzheimer’s disease.
Next Steps
Going forward, Dr. Kurmiek hopes to be the most effective lifestyle intervention in reducing bioenergy age. For example, eating a low-carb diet may help you maintain a healthy metabolism, but how low is carbohydrate consumption?
The study also points to cheap and rapid testing that can determine acylcarnitine levels in humans.
“We are fortunate that these blood tests have developed to identify metabolic and mitochondrial disorders in newborns, and that they will also help assess the age of a person’s bioenergy,” Dr. Krumsiek said.
“If we can reuse this technology for older adults, it could provide a way to start personalized treatments sooner.”
About this bioenergy age and Alzheimer’s disease research news.
author: Barbara Prempe
sauce: Weil Cornell University
contact: Barbara Prempe – Weil Cornell University
image: This image is credited to Neuroscience News
Original research: Open access.
“Individual bioenergy capabilities as a potential source of Alzheimer’s disease resilience” by Jan Krumsiek et al. Natural Communication
Abstract
Individual bioenergy capabilities as a potential source of Alzheimer’s disease resilience
Brain glucose intake is an early presymptomatic symptom of Alzheimer’s disease (AD), with symptoms-free periods that may reflect individual differences in metabolic resilience.
We propose a systematic “bioenergy ability,” which is the individual’s ability to maintain energy homeostasis under pathological conditions.
Fasting serum acylcarnitine profiles from the AD Neuroimaging initiative were used as a blood-based readout of this ability to identify subgroups with distinct clinical and biomarker presentations of AD.
Our data suggest that improving beta oxidation efficiency may slow bioenergy aging and disease progression.
The putative therapeutic effect of targeting bioenergy capabilities was comparable to the effects of recently approved anti-amyloid therapy, particularly in individuals with specific mitochondrial genotypes associated with coxynylcarnitine metabolism.
Taken together, our findings provide evidence that bioenergy health may be therapeutically enhanced.
Additionally, existing clinical assays can be used to monitor bioenergy capabilities via blood acylcarnitine measurements.
