Scientists in the United Kingdom have discovered how a key chemical disrupts brain cells in a common type of dementia. Moreover, the researchers discovered that the insult leads to a chain effect throughout the brain.
Researchers found that brain tissue from people with dementia with Lewy Bodies (DLB) contained a particular form of protein in vital parts of neurons that connect cells. Their findings suggest that this destructive protein may jump from one cell to another through these connections.
DLB is the second most common type of progressive dementia after Alzheimer’s disease dementia and attacks brain regions involved in thinking, memory, and movement (motor control). Scientists say the new findings shed light on the causes of DLB and will help to accelerate the search for a treatment as currently there is no cure for DLB.
The study, co-led by the University of Edinburgh, focused on synapses, the shared connection points between brain cells that allow chemical and electrical signals to flow between cells. These signals are vital for transmitting nerve messages and forming memories, and are key to brain health.
Researchers showed that synapses in five people who had died with DLB contained clumps of the damaging protein, known as alpha-synuclein, which could contribute to dementia symptoms. Toxic alpha-synuclein was spotted in both sides of the synapses, suggesting that it may jump between cells through these connections. This discovery reveals how damage could be spread through the brain.
Similar findings were not seen in brain tissue from people who had died with Alzheimer’s disease or those without dementia.
New imaging technology aided the discovery as scientists were able to view detailed images of over one million single synapses. Individual synapses are around 5,000 times smaller than the thickness of a sheet of paper. The researchers write that this study was the first to use the sophisticated technology for study of DLB.
Although alpha-synuclein clumps had been previously identified in DLB, their effects on synapses were unknown because of difficulties in studying them due to their tiny size.
“DLB is a devastating condition and our findings suggest that it is at least partly driven by damage to synapses. These discoveries should invigorate the search for therapies aimed at reducing synaptic damage and open the possibility of targeting the spread of alpha-synuclein through the brain, which could stop disease progression in its tracks,” said study leader Professor Tara Spires-Jones.
Dr. Rosa Sancho, head of research at Alzheimer’s Research UK, said: “This exciting research using cutting-edge technology sheds new light on the progression of DLB in the brain. The results provide convincing, measurable and visual evidence that toxic alpha-synuclein is disrupting synapses that could potentially contribute to the devastating symptoms of the disease.
“We are extremely pleased our funding has helped produce these important results which demonstrate potential avenues for much-needed new treatments for people who are living with DLB.”
Source: University of Edinburgh