LATEST! Alzheimer's breakthrough as researchers may have discovered cause disease and search for a treatment

Researchers have made a major breakthrough in discovering how Alzheimer's is caused - and say it could lead to new treatments.

The new study shows that our immune system, which protects our bodies from foreign invaders, plays a part in the debilitating disease.

However, they warn the exact role of immunity in the disease is still a mystery.
The Duke University study in mice found that in Alzheimer's disease, certain immune cells that normally protect the brain begin to abnormally consume an important nutrient: arginine.

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Blocking this process with a small-molecule drug prevented the characteristic brain plaques and memory loss in a mouse model of the disease.

Published April 15 in the Journal of Neuroscience, the new research not only points to a new potential cause of Alzheimer's but also may eventually lead to a new treatment strategy.

'If indeed arginine consumption is so important to the disease process, maybe we could block it and reverse the disease,' said senior author Carol Colton, professor of neurology at the Duke University School of Medicine, and a member of the Duke Institute for Brain Sciences.

'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,'

The brains of people with Alzheimer's disease show two hallmarks - 'plaques' and 'tangles' - that researchers have puzzled over for some time.

Plaques are the build up of sticky proteins called beta amyloid, and tangles are twisted strands of a protein called tau.

In the study, the scientists used a type of mouse, called CVN-AD, that they had created several years ago by swapping out a handful of important genes to make the animal's immune system more similar to a human's.
Compared with other mice used in Alzheimer's research, the CVN-AD mouse has it all: plaques and tangles, behavior changes, and neuron loss.

In addition, the gradual onset of these symptoms in the CVN-AD mouse gave researchers a chance to study its brain over time and to focus on how the disease begins, said the study's first author Matthew Kan, an MD/PhD student in Colton's lab.

Looking for immune abnormalities throughout the lifespan of the mice, the group found that most immune system components stayed the same in number, but a type of brain-resident immune cells called microglia that are known first responders to infection begin to divide and change early in the disease.
he group found CD11c microglia and arginase, an enzyme that breaks down arginine, are highly expressed in regions of the brain involved in memory, in the same regions where neurons had died.

Blocking arginase using the small drug difluoromethylornithine (DFMO) before the start of symptoms in the mice, the scientists saw fewer CD11c microglia and plaques develop in their brains.
These mice performed better on memory tests.

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