Gene that increases Alzheimer's disease risk was also found to disrupt brain cells, said researchers. Scientists say the findings shed light on the causes of the disease and will help to accelerate the search for a treatment.
The study, led by Professor Tara Spires-Jones at the University of Edinburgh, focused on synapses - connections between brain cells that allow the flow of chemical and electrical signals. These signals are vital for forming memories and are key to brain health, experts say.
Researchers showed that synapses in people who had died with Alzheimer's contained clumps of clusterin, which could contribute to dementia symptoms. These synapses also contained clumps of amyloid beta, the damaging protein that is found in the brains of people with Alzheimer's. People with a common risk gene, called apolipoprotein E4, had more clusterin and amyloid beta clumps in their synapses than people with Alzheimer's without the risk gene.
Synapse loss in Alzheimer's disease was previously established, but the clumping of damaging proteins together in synapses was unknown until now because of difficulties in studying them due to their tiny size.
Alzheimer's disease is the most common form of dementia, affecting around 500,000 people in the UK. It can cause severe memory loss and there is no cure.
Professor Spires-Jones, Programme Lead at the UK Dementia Research Institute at the University of Edinburgh, said: "We have identified another player in the host of proteins that damage synapses in Alzheimer's disease. Synapses are essential for thinking and memory, and preventing damage to them is a promising target to help prevent or reverse dementia symptoms. This work gives us a new target to work towards in our goal to develop effective treatments."