Various prescription medications are pictured in a file photo. By finding a link that can now be isolated and blocked by a small molecular inhibitor developed by Ferguson, doctors may be able to develop more successful medication for depression by treating anxiety.
OTTAWA – Scientists have always known that anxiety and depression were linked. They just couldn't prove it in the brain -- until now.
A discovery about the cellular link between anxiety and depression by Canadian university researchers may provide a better way to treat depression, a condition that affects as much as 20 per cent of this country's population.
"We hadn't known the mechanism by which these two things were physically related," said Stephen Ferguson, a researcher at Robarts Research Institute at the University of Western Ontario.
"Basically, what we're finding is that there's talk between these two receptor systems in the brain, and that if you activate the one receptor system the other becomes sensitized."
The findings, published in a study released Sunday in the journal Nature Neuroscience, also reveal a way to block this link in the brain and potentially reduce anxiety and improve the way depression is treated.
It all has to do with the receptor systems -- made up of proteins on brain cells, which react to neurotransmitters and are the target of depression medication because they are involved in perception and mood -- and the way they activate multiple brain functions.
By finding a link that can now be isolated and blocked by a small molecular inhibitor developed by Ferguson, doctors may be able to develop more successful medication for depression by treating anxiety.
"Most drugs that are used for the treatment of depression block everything the receptor does and what we're doing is blocking one single function, which may allow for the development of drugs with less side effects in the future," said Ferguson.
"If we can block this anxiety-related increase in depression by targeting just one cellular process that these receptors are activating, maybe we can leave other ones intact, reducing the intolerable side effects of these drugs," he said.
The research was conducted on mice and took about five years to complete. It also involved Ferguson's colleagues from the University of Western Ontario, where he teaches pharmacy and physiology, and others, including Carleton University neuroscience professor Hymie Anisman.
Anisman said anxiety is often a precursor to depression, or can make it worse. He said depression medication typically only works for about 60 per cent of patients.
"Now that we know where things are happening in the brain, now we can target these sites to develop treatments to ameliorate anxiety or depression in a way that's better than the ones that currently exist," said Anisman.
The study was funded in part by the Canadian Institutes of Health Research.
"We hadn't known the mechanism by which these two things were physically related," said Stephen Ferguson, a researcher at Robarts Research Institute at the University of Western Ontario.
"Basically, what we're finding is that there's talk between these two receptor systems in the brain, and that if you activate the one receptor system the other becomes sensitized."
The findings, published in a study released Sunday in the journal Nature Neuroscience, also reveal a way to block this link in the brain and potentially reduce anxiety and improve the way depression is treated.
It all has to do with the receptor systems -- made up of proteins on brain cells, which react to neurotransmitters and are the target of depression medication because they are involved in perception and mood -- and the way they activate multiple brain functions.
By finding a link that can now be isolated and blocked by a small molecular inhibitor developed by Ferguson, doctors may be able to develop more successful medication for depression by treating anxiety.
"Most drugs that are used for the treatment of depression block everything the receptor does and what we're doing is blocking one single function, which may allow for the development of drugs with less side effects in the future," said Ferguson.
"If we can block this anxiety-related increase in depression by targeting just one cellular process that these receptors are activating, maybe we can leave other ones intact, reducing the intolerable side effects of these drugs," he said.
The research was conducted on mice and took about five years to complete. It also involved Ferguson's colleagues from the University of Western Ontario, where he teaches pharmacy and physiology, and others, including Carleton University neuroscience professor Hymie Anisman.
Anisman said anxiety is often a precursor to depression, or can make it worse. He said depression medication typically only works for about 60 per cent of patients.
"Now that we know where things are happening in the brain, now we can target these sites to develop treatments to ameliorate anxiety or depression in a way that's better than the ones that currently exist," said Anisman.
The study was funded in part by the Canadian Institutes of Health Research.
No comments:
Post a Comment