Hope to halt dementia
Drug might radically change outlook for people with Alzheimer’s
DEMENTIA is now the disease we fear more than any other, even cancer.
As Dr James Pickett, head of research at the Alzheimer’s Society, says: “It is currently the only one of the top 10 killers that we can’t cure, prevent or even slow down.”
But a new trial is under way of a drug, miridesap, which, if successful, could radically change the outlook for those affected with Alzheimer’s, the most common form of dementia.
“Potentially the biggest thing since sliced bread,” is how the man who developed the drug, Professor Sir Mark Pepys, an immunologist and director of the Wolfson Drug Discovery Unit at University College London, describes it.
Miridesap targets a protein called serum amyloid P (SAP) component which is newly suspected to play a key role in Alzheimer’s.
Most of the drugs previously tested have targeted amyloid plaques, microscopic tangles of abnormal protein which are found wrapped around brain cells in great quantities in those with Alzheimer’s.
The belief was that these tangles play a key part in the death of brain cells and the loss of memory and cognition that characterise the disease.
SAP is being targeted now as it has a double negative effect, destroying brain cells as well as protecting (harmful) amyloid.
Pepys believes that SAP is a vital mechanism in Alzheimer’s and might explain why previous drugs that only targeted amyloid have not worked. Miridesap, it is hoped, will clear the amyloid, too.
“Amyloid should be cleared from the body by macrophages that eat up and destroy general debris from around the cells,” says Pepys.
“But SAP puts a protective coating on amyloid so it can’t be cleared.”
Miridesap resembles the outer coating of amyloid so SAP locks onto it instead and, deprived of its protective cover, amyloid is then ingested in the liver. A small trial in 2005 found that miridesap cleared all SAP from the blood and also from the fluid around the brain in those with dementia.
The hope is that in the absence of SAP, macrophages will then get to work on tackling the 100mg or so of amyloid that accumulates in the brains of people with Alzheimer’s.
The plan is to recruit 100 volunteers with mild Alzheimer’s who will try the drug or a placebo for a year.
Those on the trial will be taught how to self-inject the drug three times a day.
During that year the volunteers will undergo multiple tests including brain scans to check on any shrinkage, and blood tests to check on SAP levels.
Pepys stresses that it won’t be “some miracle cure, but what we hope is that it might halt the disease”.
The drug is also being tested in a separate trial on those with amyloidosis – a rare potentially fatal disease in which amyloid builds up in organs
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| throughout the body.
Clive Ballard, a professor of age-related diseases at Exeter University, believes that in Alzheimer’s it may be that amyloid is important early on in the process and becomes less so later.
This, he says, may explain why previously amyloid-reducing drugs have not shown much effect.
And it is why he believes that miridesap may turn out to have a preventative role. |
A NEW drug in the pipeline to treat dementia won’t be a ‘miracle cure’, but it may help halt the disease.|