Australian researchers on Friday said they have replicated a crucial brain process that pointed to a potential pathway in slowing the development of Alzheimer's disease.
Overcoming the loss of a process in the brain called "RNA editing" may slow the progress of the major neurological condition and other synaptic disorders, the University of Technology Sydney said in a statement late Friday.
"RNA editing" is a genetic mechanism that modifies proteins essential in the connection between brain nerve cells called synapses, it said. RNA editing is deregulated in the brains of Alzheimer's disease patients, but whether that can cause disease is unknown.
University researchers "replicated this deregulated process in the brains of mice, and discovered it led to the loss of synapses, as occurs in Alzheimer's". Alzheimer's is a progressive, irreversible neurological disorder and the most common form of dementia, with most patients older than 65.
"Understanding mechanisms leading to synapses loss is essential to understand how patients suffering from Alzheimer's disease start losing their memory capacities and how to prevent this from happening," said Professor Bryce Vissel, senior author of the findings published in scientific journal Molecular Brain.
"Our study is extremely important because we now have shown a mechanism that can lead to loss of synapses as occurs in Alzheimer's disease."
Dr Gary Morris, a scientist who contributed to the study, said that because "synapses are important for learning, the loss of these synapses leads to memory loss".
"Our study suggests that if we can overcome the loss of RNA editing in the brain, we may potentially be able to slow the disease."
Vissel said the researchers' next step is "to see if they can rescue synapses and memory deficits in Alzheimer's disease by overcoming the loss of RNA editing in the Alzheimer's brain".
"We have good reason to think that this could ultimately be a highly beneficial approach for solving Alzheimer's and potentially other neurodegenerative diseases such as Parkinson's," Vissel said.