Removing protein may restore earliest sign of Alzheimer’s
Tuesday 28 March, 2017

Removing protein may restore earliest sign of Alzheimer’s

Published On: Thu, Dec 1st, 2011 | Alzheimer's | By BioNews

Loss of smell, which is one of the earliest impairments caused by Alzheimer’s disease, can be restored by removing a plaque-forming protein in a mouse model of the disease, a new study has suggested.

According to a study led by a Case Western Reserve University School of Medicine researcher, the protein known as amyloid beta causes the loss.

“The evidence indicates we can use the sense of smell to determine if someone may get Alzheimer’s disease, and use changes in sense of smell to begin treatments, instead of waiting until someone has issues learning and remembering,” Daniel Wesson, lead investigator of the study, said.

“We can also use smell to see if therapies are working,” he said.

Smell loss can be caused by a number of ailments, exposures and injuries, but since the 1970s, it has been identified as an early sign of this disease. The new research highlights how and where in the brain this happens, and that the impairment it can be treated.

“Understanding smell loss, we think, will hold some clues about how to slow down this disease,’ Wesson said.

There is currently no effective treatment or cure for the disease, marked by eroding senses, cognition and coordination, leading to death.

The researchers found that just a tiny amount of amyloid beta, too little to be seen on today’s brain scans, causes smell loss in mouse models.

Amyloid beta plaque accumulated first in parts of the brain associated with smell, well before accumulating in areas associated with cognition and coordination.

Early on, the olfactory bulb, where odour information from the nose is processed, became hyperactive.

Over time, however, the level of amyloid beta increased in the olfactory bulb and the bulb became hypoactive. Despite spending more time sniffing, the mice failed to remember smells and became incapable of telling the difference between odours.

The same pattern is seen in people with the disease. They become unresponsive to smells as they age.

While losses in the olfactory system occurred, the rest of the mouse model brain, including the hippocampus, which is a centre for memory, continued to act normally early in the disease stage.

“This shows the unique vulnerability of the olfactory system to the pathogenesis of Alzheimer’s disease,” Wesson added.

The team then sought to reverse the effects. Mice were given a synthetic liver x-receptor agonist, a drug that clears amyloid beta from the brain.

After two weeks on the drug, the mice could process smells normally, and after withdrawal of the drug for one week, the impairments returned.

The study has been published in The Journal of Neuroscience.

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