In order for memory to function correctly, nerve cells must be able to communicate effectively with each other. Many important proteins in the brain ensure that this communication is maintained between healthy nerve cells by monitoring the junctions, or synapses, between cells. This is also the location of production of amyloid-beta, which accumulates as plaques in Alzheimer's disease.

The gene PSEN1 is responsible for the protein presenilin1. Faulty versions of this gene are known to be linked to early onset Alzheimer's disease. This new study shows that presenilin1 plays an important role in the functioning of synapses between nerve cells and suggests that the faulty protein disrupts communication between cells, thus affecting memory. The work also suggests that presenilin1 is linked with amyloid-beta and production of toxic plaques in the brain during Alzheimer's disease.

Alzheimer's Society comment:

'This study shows that a gene linked with early onset Alzheimer's plays an important role in storing memory. This is an interesting finding which could lead to new research into how we can develop drug treatments that target this area.

One million people will develop dementia in the next 10 years. We must act now. We need a national plan for dementia research and a tripling of investment to see research translated into better treatments for millions of people.  

Dementia is not a natural part of ageing; it is caused by diseases of the brain. 15,000 people under 65 live with dementia in the UK.'

 
Professor Clive Ballard
Director of Research
Alzheimer's Society