A study published in the January 13, 2010 issue of the Journal of Neuroscience links a loss of smell function in Alzheimer's disease (AD) model animals with amyloid β (protein) accumulation in the brain, a distinguishing hallmark of Alzheimer's disease. Research conducted by NYU Langone Medical Center suggests that olfactory dysfunction, a common symptom of AD, may serve as an early diagnostic tool for the disease.
The formation of amyloid plaques and neurofibrillary tangles are believed to contribute to the degradation of the neurons in the brain and the subsequent symptoms of AD. In this newly published study, NYU Langone scientists used genetically engineered mice, which developed amyloids in their brains, reflecting a progressive Alzheimer's disease pathology similar to humans. They found that Alzheimer's disease amyloid pathology occurs first in a region of the mouse brain responsible for smelling—which is directly above their noses. This pathology also coincided with the animals having abnormal abilities to smell. The mice with a high concentration of amyloid in their brains had to sniff odors longer to "learn" them than mice with less amyloid. They also had problems differentiating between odors.
As the article in the Journal of Neuroscience suggests, since the behavioral symptoms of AD often occur early in life, it is possible that this new olfactory method, looking at olfactory perception across multiple presentations of the same odor, may be advantageous in early detection of Alzheimer's -- prior to substantial degeneration of the brain.