Boredom, routine no help to brain disorder sufferers

BANISHING boredom could aid the recovery of memory in patients with Alzheimer’s and other degenerative brain diseases, new research suggests.

Scientists made the discovery after keeping mice with an artificially-induced Alzheimer’s-like illness in an “enriched environment”.

The animals were given an exercise treadmill, an array of colourful toys with various shapes and textures that were changed daily, and the companionship of other mice.

Subjected to memory tests, the stimulated rodents fared far better than other mice held in standard bare cages.

The mice living in stimulating conditions also showed a surprising ability to recover long-term memories, weeks after training.

Study leader Dr Li-Huei Tsai of the Massachusetts Institute of Technology said: “This recovery of long-term memory was really the most remarkable finding. It suggests that memories are not really erased in such disorders as Alzheimer’s, but that they are rendered inaccessible and can be recovered.”

When the researchers studied the brains of the animals they found no evidence of neurons re-growing or new cells forming.

However, there were both physical and biochemical signs of an increased number of connections between neurons.

Reinforcement of neural connection points called synapses is known to be fundamental to the mechanism of memory.

The research, reported in the journal Nature, suggests elderly patients with dementia may do better if their lives are colourful and interesting.

In contrast, monotonous routines of the kind that shape everyday life in many homes could be harmful.

Dr Tsai added: “I believe that these findings could have particular significance for treatment of people who already have advanced neuro-degenerative disease.

“Most current treatments seem to be aimed at affecting the early stages of the disease. But our mouse model shows that even when there has been a significant loss of neurons, it is still possible to improve learning and memory.”

The scientists manipulated a gene called p25 to produce symptoms in the mice very similar to Alzheimer’s in humans. Their brains shrink, and they suffer severe learning and memory impairment accompanied by the loss of synapses.

Scientists hope further work will lead to drugs that use this principle to enhance learning and memory.