Mentally taxing tasks really can do your head in -- by causing genetic damage to nerve cells, research has shown.
But the process is perfectly normal and the damage quickly repaired in healthy brains, a study found.
The problem arises when the brain is not healthy. In that case the repairs are not made fast enough, leading to illnesses such as Alzheimer's, evidence suggests.
Scientists working with mice discovered that stimulating the animals disrupted DNA in their neurons.
Mentally taxing tasks could lead to illness in unhealthy brains
The particular type of damage, called a double-strand break, or DSB, has long been suspected of driving age-related illnesses such as Alzheimer's.
In their experiments, the researchers found that DSBs were a normal - and perhaps even necessary - part of learning.
Two groups of mice were allowed to explore a new environment filled with unfamiliar sights, smells and textures.
One group consisted of healthy normal animals; the other was genetically modified to simulate key aspects of Alzheimer's disease.
The normal mice showed an increase in DSB damage after the mental stimulation of unfamiliar surroundings. But after being returned to their home environment, DSB levels rapidly dropped as the breaks were repaired.
The Alzheimer's mice had more DSBs to start with, and their levels rose even higher when their brains were stimulated. In these animals, it took much longer for DNA repairs to be carried out.
"We were initially surprised to find neuronal DSBs in the brains of healthy mice," said researcher Dr Elsa Suberbielle, from the Gladstone Institute of Neurological Disease in San Francisco, US.
"But the close link between neuronal stimulation and DSBs, and the finding that these DSBs were repaired after the mice returned to their home environment, suggest that DSBs are an integral part of normal brain activity.
"We think that this damage-and-repair pattern might help the animals learn by facilitating rapid changes in the conversion of neuronal DNA into proteins that are involved in forming memories."
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A known hallmark of Alzheimer's - accumulating amyloid-beta protein in the brain - increases the number of neurons with DSBs, the scientists learned.
The findings appear in the latest issue of the journal Nature Neuroscience.
Treatment with the epilepsy drug levetiracetam reduced DSB damage in the mice, as did reducing levels of another brain protein called tau.
Previous studies have shown that levetiracetam can improve neural communication and memory in patients with early-stage Alzheimer's.
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Study leader and senior Gladstone investigator Dr Lennart Mucke said: "Currently, we have no effective treatments to slow, prevent or halt Alzheimer's, from which more than five million people suffer in the United States alone.
"The need to decipher the causes of Alzheimer's and to find better therapeutic solutions has never been more important or urgent.
"Our results suggest that readily available drugs could help protect neurons against some of the damages inflicted by this illness.
"In the future, we will further explore these therapeutic strategies. We also hope to gain a deeper understanding of the role that DSBs play in learning and memory, and in the disruption of these important brain functions by Alzheimer's disease."