Removing amyloid beta can restore sense of smell in mouse model of Alzheimer's

Published on November 30, 2011 at 11:51 PM · 1 Comment

One of the earliest known impairments caused by Alzheimer's disease - loss of sense of smell - can be restored by removing a plaque-forming protein in a mouse model of the disease, a study led by a Case Western Reserve University School of Medicine researcher finds.

The study confirms that the protein, called 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," said Daniel Wesson, assistant professor of neuroscience at Case Western Reserve and lead investigator. "We can also use smell to see if therapies are working."

A description of the research is published in the Nov. 2 issue of The Journal of Neuroscience.

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.

"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. 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.

Read in | English | Español | Français | Deutsch | Português | Italiano | 日本語 | 한국어 | 简体中文 | 繁體中文 | Nederlands | Русский | Svenska | Polski
Comments
  1. Ann Hanley Ann Hanley United States says:

    I was diagnosed with PD 4 years ago, had no "smell" for 10 years and in July after a 30 day chelation my "smell" came back. I really feel this is important, could somebody explain the significence please ?

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News-Medical.Net.
Post a new comment
Post