Researchers have discovered that limiting a certain enzyme can have a dramatic impact in protecting against the effects of Alzheimer’s disease. Much of the historical research into Alzheimer’s disease has focused on plaques that form in the brain thanks to the accumulation of too much amyloid proteins.
Once again looking at how suppressing PDE4B might affect the brain, the UK team genetically modified mice with Alzheimer’s and amyloid plaques in the brain to have reduced PDE4B activity.
Finally, the team observed that mice with less PDE4B activity had less inflammation in their brains than those with more of the enzyme – another hallmark of AD. Because all of these effects were found in mice that already had Alzheimer’s – and the accompanying amyloid plaques – but had significant improvement in symptoms, the researchers say that further investigation into how to limit PDE4B in human patients with the condition could lead to new treatment pathways.
“These results offer real hope for the development of new treatments that will benefit patients with Alzheimer’s disease in the future,” said LU’s Neil Dawson, a co-author of the study.
“Reducing the activity of the PDE4B enzyme had a profound protective effect on memory and glucose metabolism in the AD mouse model, despite these mice showing no decrease in the number of amyloid plaques in the brain,” he said.
“This raises the prospect that reducing PDE4B activity may protect against cognitive impairment not only in Alzheimer’s disease but also in other forms of dementia, such as Huntington’s disease.” Huntington’s is also marked by a build-up of plaques in the brain.