Loss of Sense of Smell Reversed In Mouse Model of Alzheimer’s Disease

Loss of Sense of Smell Reversed In Mouse Model of Alzheimer’s Disease

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

Currently 5.3 million Americans suffer from Alzheimer’s disease and the number is expected to triple to 16 million by 2050, according to the Alzheimer’s Association.

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

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 center 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.

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.

After withdrawal of the drug for one week, impairments returned.

The researchers are now following-up on these discoveries to determine how amyloid spreads throughout the brain, to learn methods to slow disease progression.

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