New Drugs Could Stop One Form Of Dementia 'In Its Tracks'
New drugs for one of the most common forms of dementia could be on the horizon after scientists discovered how the illness spreads.
Researchers hope the drugs could stop dementia with Lewy bodies, also called DLB, 'in its tracks' by targeting a key chemical called alpha-synuclein.
The rogue protein is one of four types that is believed to be behind the devastating neurological disorder. It disrupts brain cells in dementia with Lewy bodies - which is the same kind that Robin Williams was posthumously diagnosed with after taking his own life in 2014.
Brain tissue from people who died from DLB showed the protein builds up in vital parts of neurons that connect cells. The hope is that these findings, produced by an international team led by Edinburgh University, can shed light on the causes of DLB and speed up the search for a treatment.
After Alzheimer's and vascular dementia, DLB is the third most common form of dementia, affecting approximately 100,000 people in the UK and accounting for about four percent of all recorded dementia. It can cause severe memory loss as well as movement problems and there is currently no cure.
This latest study focused on synapses, the connections between nerve cells that form memories. Synapses also allow chemical and electrical signals to flow between cells and, according to experts, are vital for brain health.
Professor Tara Spires-Jones, who heads up the UK Dementia Research Institute at Edinburgh University and was co-leader of the study, said: "DLB is a devastating condition. Our findings suggest it's 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."
The study's research showed how synapses in five people who had died with DLB contained clumps of alpha-synuclein.
The toxic protein was spotted in both sides of the synapses, which suggests it may jump between cells via these connections and demonstrates how damage could then be spread throughout the brain.
Interestingly, the protein was not seen in the brain tissue of those with Alzheimer's disease or people without any type of the illness.
The discovery was made with extremely powerful scanning devices used in DLB for the first time, which provided detailed images of over one million single synapses - each of which is 5,000 times smaller than the thickness of a sheet of paper.
Featured Image Credit: PA