Cell energy systems change in aging mouse brain nerve endings
The voltage across mitochondrial membranes fell 21% at 20 months but rose 24% at 24 months, compared with young mice.
Our read
Mechanisms- Studied:
- Experiments in mice of different ages, against young mice
- What changed:
- Mitochondrial membrane voltage fell 21% at 20 months and rose 24% at 24 months compared with young mice
- The catch:
- Energy production in intact brains was not measured
- Why it’s aging research:
- It studies organisms or tissues that aged naturally.
Editor of record: Boris Djordjevic · AgingResearch.News
In an animal experiment, researchers studied mice aged 3, 10, 20 and 24 months, examining isolated nerve-ending preparations from the brain’s cortex. They tested mitochondria, the cell structures that supply energy, and measured production of reactive oxygen molecules.
The voltage across mitochondrial membranes fell 21% at 20 months and rose 24% at 24 months, compared with young mice. At 24 months, both energy production and its efficiency declined. Production of superoxide, a reactive oxygen molecule, increased with age. The authors concluded that mitochondrial function became significantly impaired at 20 months. They suggested that compensatory mechanisms might emerge at more advanced ages, even as the mitochondria’s ability to supply energy seemed severely compromised.
Why it matters
Energy supply at nerve-cell connections bears on how the brain changes with age. The study raises the question of whether compensatory responses can offset age-related mitochondrial dysfunction.
Caveats
The results came from isolated mouse nerve-ending preparations; they do not establish effects in intact brains or in people.
- Hydrogen peroxide
- Oxidative phosphorylation
- Oxidative stress and ROS signaling
- Superoxide
- ATP synthesis
- Mice
The paper
Dynamic changes in mitochondrial function in brain cortex synaptosomes during aging
Consejo Nacional de Investigaciones Científicas y Técnicas
Journal of Bioenergetics and Biomembranes, May 9, 2026, Open access
Comments
Be the first to comment.