A Treat For A Sign Of Alzheimer

The cruel disease, Alzheimer effects on the brain. It took the name from Alois Alzheimer the German psychiatrist whom first described the disease. One of the first parts in the brain affected by the disease is the part responsible for smelling.

The researchers of Case Western Reserve University School of Medicine, have reached for the reason of this effect. They made a research on a mouse which suffers from the disease, they reached for the responsible protein for the problem. They found that the smell sense is lost due to the presence of the protein that is called amyloid beta. They also reached that by removing that protein, the smell sense can be restored.

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 shows how and where in the brain this happens, and that the impairment it can be treated.
There is currently no effective treatment or cure for the disease, marked by eroding senses, cognition and coordination, leading to death.
Currently 5.3 million Americans suffer from Alzheimer’s and the number is expected to triple to 16 million by 2050, according to the Alzheimer’s Association.
Wesson worked with Anne H. Borkowski, a researcher at the Nathan S. Kline Institute in Orangeburg, N.Y., Gary E. Landreth, professor of neuroscience at Case Western Reserve School of Medicine, and Ralph A. Nixon, Efrat Levy and Donald A. Wilson, of the New York University School of Medicine.
They 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 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. 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.
Wesson and his team 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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