Dementia ‘halted in mice brains’
The team at Duke University, in the US, showed immune cells which start attacking nutrients in the brain may be a trigger for the disease.
They say their findings could open up new avenues of research for a field that has not developed a single drug to slow the progression of the disease.
Experts said the findings offered new hope of a treatment.
The researchers indentified microglia - normally the first line of defence against infection in the brain - as major players in the development of dementia.
They found some microglia changed to become exceptionally adept at breaking down a component of protein, an amino acid called arginine, in the early stages of the disease.
As arginine levels plummeted, the immune cells appeared to dampened the immune system in the brain.
Stopping dementia
In mouse experiments, a chemical was used to block the enzymes that break down arginine.
They showed fewer of the characteristics of dementia such as damaged proteins collecting in the brain and the animals performed better in memory tests.
One of the researchers, Dr Matthew Kan, said: “All of this suggests to us that if you can block this local process of amino acid deprivation, then you can protect the mouse, at least from Alzheimer’s disease.
"We see this study opening the doors to thinking about Alzheimer’s in a completely different way, to break the stalemate of ideas in Alzheimer’s disease.”
However, the findings do not suggest that arginine supplements could combat dementia as the boosted levels would still be broken down.
'Hope’
Dr James Pickett, from the Alzheimer’s Society said the study was “offering hope that these findings could lead to new treatments for dementia”.
He added: “This study in animals joins some of the dots in our incomplete understanding of the processes that cause Alzheimer’s disease, in particular around the role played by the immune system.”
Dr Laura Phipps, from Alzheimer’s Research UK, said the study was “interesting” and shed “more light on the mechanisms of immune system involvement in Alzheimer’s”.
But she cautioned clinical trials in people were still needed and that “the findings do not suggest that supplementation of the amino acid could mirror the benefits seen in these mice”.
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