Reversal of Early Sign of Alzheimer’s Disease

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The loss of sense of smell or olfaction, which was one of the earliest known impairments caused by Alzheimer’s disease, can be restored by removing a plaque-forming protein in a mouse model of the disease, according to a study led by a Case Western Reserve University School of Medicine researcher. The study confirms that the protein, called amyloid beta, causes the loss.

Daniel Wesson, assistant professor of neuroscience at Case Western Reserve and lead investigator stated that the findings indicate 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, as well as knowing if therapies are working. He also stated that understanding smell loss will hold some clues about how to slow down this disease.

Currently, there is no effective treatment or cure for the disease, which is displayed by eroding senses, cognition and coordination, leading to death.

Wesson and his team found out that 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, before accumulating in areas associated with cognition and coordination.

Early on, the olfactory bulb, where smell 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, identify, and detect smells and became incapable of differentiating odors.

This same pattern of olfaction loss is seen in people with Alzheimer’s. They become unresponsive to smells as age progresses. While losses in the olfactory system occurred, the rest of the mouse model brain (including the hippocampus being the center for memory) continued to act normally early in the disease stage. Wesson concluded that this shows the unique vulnerability of the olfactory system to the pathogenesis of Alzheimer’s disease.

The team then attempted to reverse the effects. Mice were administered 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 and distinguish smells normally. After withdrawal of the drug for a week, the olfactory impairments returned.

Wesson and his team are now following-up and expanding on these findings to determine how amyloid spreads throughout the brain, to learn methods of slowing progression of Alzheimer’s disease.




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