Brain energy shortage may limit learning with age

Mitochondria (the cell’s energy-producing structures) have long been associated with aging. But their specific role in cognitive flexibility was unclear. The researchers had mice of different ages perform a task where the rules changed halfway through: what worked before suddenly no longer applied. Older mice struggled significantly more than younger ones.

Not the dendrites, but the synapse

Surprisingly, the decline did not correspond to the most obvious candidates. Loss of small dendrites (the receiving extensions of neurons) had no measurable impact on task performance. Changes in astrocytes (support cells surrounding synapses) showed no association either.

What did matter: the mitochondria located in presynaptic terminals, the sites where neurons transmit a signal. Mice that performed poorly on the task had less functional mitochondria at precisely those locations. The position of the energy deficit turned out to be more specific than previously thought.

Small sample, preliminary conclusions

The study was conducted in mice and the number of animals was limited. The researchers acknowledge this themselves: the group was too small to draw definitive conclusions about the proteins and genes involved. The findings are preliminary and require follow-up in larger groups and in other species.

For longevity science, the direction is noteworthy. Mitochondria in presynaptic terminals have received little attention as a specific target for cognitive decline. If further studies confirm this link, it could open a potential avenue for interventions aimed at preserving cognitive flexibility with age.

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