New approach in treating dementia: neuroreceptor improves memory

Researchers at FAU and at Heinrich Heine University Düsseldorf have discovered a mechanism in the brain that improves memory. In addition, the researchers identified a gene that allows for predictions about possible memory disorders in old age. The results of their research open up new possibilities for the diagnosis and treatment of dementia. The researchers have recently published their study in the journal ‘Proceedings of the National Academy of Science USA’ (*).

More and more people are living to be older and older, and an increasing number are suffering with dementia. Memory loss decreases quality of life and can – such as in the case of Alzheimer’s – result in a complete loss of autonomy. So far, we are not able to stop or reverse these cognitive penalties of old age. Researchers at FAU and at the University of Düsseldorf have now discovered a mechanism in the brain that could change this.

In a healthy, young brain it only plays an unimportant role, but in older people, its genetic make-up determines memory capacity and thus whether a person will suffer from dementia: the neurokinin3 receptor. This is a molecule that causes the messenger substance acetylcholine to be released during signal transmissions of peptides in the brain. As the scientists led by PD Dr. Maria A. De Souza Silva of the University of Düsseldorf and Prof. Dr. Christian P. Müller of FAU have now discovered, the neurokinin3 receptor controls the release of the neurotransmitter acetylcholine in the brain.

Function of receptor shown in aged rats

This neurotransmitter has long been associated with controlling concentration and memory. ‘In our study we have shown that the receptor activates the release of acetylcholine and that this improves mnemonic performance,’ Prof. Müller explains. The research group examined the influence of the receptor on memory in model experiments with aged rats.

As in older humans, the ability to retain knowledge decreases in older rats. In the experiment, the rats had to swim through a maze to find a hidden platform. In the second round it was examined how well they remembered the way: the rats failed the test, did not recognise their surroundings and had to find the way all over again. However, this was not the case in the rats whose neurokinin3 receptors had been stimulated: they found their way through the maze and to the safe platform without problems.

Transferring this experiment to humans is not easily possible, though. ‘We know that the mechanism is the same in rats and humans. But the substance that we gave the rats to stimulate the receptors does not work on humans,’ says Prof. Müller.

Genes provide further clues

In a second phase, the researchers therefore concentrated on the gene that encodes the receptor. Prof. Müller and his colleagues evaluated random samples of older people with dementia. The random samples had been collected for the research of Kompetenznetzwerk Demenzen (Competence Network Dementia), of which Universitätsklinikum Erlangen is a part. The scientists compared both the volume of the hippocampus – a region of the brain that plays an important role for memory – as well as the memory of the test subjects.

The result: the different gene variations explained the varying decrease in hippocampal volume and the variations in mnemonic ability. ‘This result underscores the significance of the neurokinin3 receptor for brain function and memory in old age,’ Prof. Müller explains. In the future, these results could aid the development of new diagnostic instruments as well as medicinal treatments for different kinds of dementia.

(*) Above quote: http://www.pnas.org/content/110/37/15097.long

Further information:

Prof. Dr. Christian P. Müller
Phone: +49 (0)9131 85 36896
christian.mueller@uk-erlangen.de