Aged mice lacking a protein showed better cognitive performance
In an animal experiment, 24-month-old mice lacking the protein cyclophilin D also produced more cellular energy than same-age mice that made it.
Limit: The experiment compared mice genetically lacking the protein rather than treating older animals
Edited by Boris Djordjevic · AgingResearch.News
In an animal experiment, 24-month-old mice lacking the protein cyclophilin D showed better cognitive performance than same-age mice that made it. Their mitochondria, the cell structures that supply energy, worked better and produced more ATP, the molecule cells use for energy. The researchers also reported closure of a pore in mitochondrial membranes that cyclophilin D can activate.
Mice lacking cyclophilin D had higher levels of a protein found at nerve-cell connections in the hippocampus, a brain region involved in memory. Lack of cyclophilin D also prevented accumulation of tau cut by the enzyme caspase-3. Tau is a protein implicated in nerve-cell damage. This effect occurred in both mitochondria and the surrounding cell fluid in hippocampal tissue.
Why it matters
Mitochondrial problems are considered a hallmark of brain aging. The findings suggest cyclophilin D may be a target for studying tau-related nerve-cell damage during aging.
Caveats
The experiment compared mice genetically lacking the protein with normal mice; it did not test a treatment in older animals or people. The abstract does not report the number of mice or how cognitive performance was assessed.
The paper
Universidad Autónoma de Chile
Free Radical Biology & Medicine, Jul 9, 2026
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