A woman suffering from Alzheimer's desease/AFP
The antibodies shut down a protein called Dkk1 that in turn stops the formation of amyloid plaque in the brain, a key factor in the progression of Alzheimer’s, said the findings in the Journal of Neuroscience.
When this plaque builds up, it leads to a loss of connection between neurons, known as synapses, in the part of the brain known as the hippocampus which handles learning and memory.
“These novel findings raise the possibility that targeting this secreted Dkk1 protein could offer an effective treatment to protect synapses against the toxic effect of amyloid-B,” said lead author Patricia Salinas of the University College London Department of Cell and Developmental Biology.
“Importantly, these results raise the hope for a treatment and perhaps the prevention of cognitive decline early in Alzheimer’s disease.”
The research has only been done in mice and more work is needed to see if it would be relevant in humans.
Previous research has shown that the autopsied brains of people with Alzheimer’s disease have higher levels of Dkk1 than normal brains, but scientists were unsure why.
The latest study on mice showed that animals exposed to antibodies against Dkk1 had more of their synapses survive than other Alzheimer’s mice that were not given the treatment.
The research was funded by Alzheimer’s Research UK and the Biotechnology and Biological Sciences Research Council.
There is no cure for Alzheimer’s, a progressive brain disease which along with other forms of dementia affects more than 35 million people worldwide.
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