Specific Antibodies Halt Alzheimer’s in Mice

Antibodies that block the process of synapse disintegration in Alzheimer’s disease have been identified, raising hopes for the development of a treatment to combat early cognitive decline in the disease.

During Alzheimer’s, a protein called amyloid-beta builds in the brain and causes the loss of synapses – the connections between brain cells.

Scientists at UCL, part-funded by Alzheimer’s Research UK, studied a second protein called Dkk1. They discovered that specific antibodies that block the function of Dkk1 completely suppressed amyloid-beta’s toxic effect on synapses. The findings are published in the Journal of Neuroscience.

Dr Patricia Salinas, from the UCL Department of Cell & Developmental Biology, who led the study, said:
“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-beta.

“Importantly, these results raise the hope for a treatment and perhaps the prevention of cognitive decline early in Alzheimer’s disease.”

Research has shown high levels of Dkk1 in brain samples from people with Alzheimer’s disease, but the significance of these findings was previously unknown. Scientists at UCL have found that amyloid-beta causes the production of Dkk1, which in turn leads to the loss of synapses in the hippocampus, an area of the brain responsible for learning and memory.

The scientists studied the progression of synapse disintegration in the hippocampus after exposure to amyloid-beta, using brain slices from mice. They were able to monitor how many synapses survived in the presence of a specific antibody that targets Dkk1, compared to how many synapses survived without the antibody.

The results showed that brain cells that were exposed to the antibody remained healthy, and the synapses remained intact.

Dr Salinas said:
“Despite significant advances in understanding the molecular mechanisms involved in Alzheimer’s disease, no effective treatment is currently available to stop the progression of this devastating disease.”

She added:
“This research identifies Dkk1 as a potential therapeutic target for the treatment of Alzheimer’s disease.”

Alzheimer’s is the most common cause of dementia, accounting for about two-thirds of cases. Currently, dementia costs the UK economy £23 billion a year – more than cancer and heart disease combined – and the number of people with the condition is expected to double within a generation.

The research was funded by Alzheimer’s Research UK and the Biotechnology and Biological Sciences Research Council, UK.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said:
“We’re delighted to have supported this study, which sheds new light on the processes that occur as Alzheimer’s develops. By understanding what happens in the brain during Alzheimer’s, we stand a better chance of developing new treatments that could make a real difference to people with the disease.

“Studies like this are an essential part of that process, but more work is needed if we are to take these results from the lab bench to the clinic. Dementia can only be defeated through research, and with the numbers of people affected by the condition soaring, we urgently need to invest in research now.”

This material has been published with the kind permission of Alzheimer Research UK.

Image reproduced from http://controlmind.info

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