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NIDCD research at AChemS Annual Meeting

What: Scientists supported by the National Institute on Deafness and Other Communication Disorders (NIDCD), one of the National Institutes of Health, will be presenting their latest research findings at the 2011 Annual Meeting of the Association for Chemoreception Sciences (AChemS).

When: April 13-17, 2011

Where: Tradewinds Grand Isle Resort, St. Petersburg, Florida

Additional Information: Research topics to be presented by NIDCD-funded scientists will include:

New Findings Suggest Novel Avenues to Explore Taste Loss in Autoimmune Diseases

Reduced taste sensitivity is a common symptom of autoimmune diseases such as Sjogren's syndrome and lupus, and it can have a negative impact on a person's nutrition. Taste sensitivity waxes and wanes along with other disease symptoms, but the mechanism by which inflammation could contribute to the loss of taste remains largely unknown. NIDCD-funded researcher Hong Wang, Ph.D., and colleagues at the Monell Chemical Senses Center, in Philadelphia, have used a mouse strain (MRL/lpr) that models lupus in humans to explore the effects of chronic inflammation on taste tissues. The investigators noted increased levels of inflammation-promoting immune system cells in the tongue tissue of MRL/lpr mice in association with lower expression levels of markers for Type II taste cells. (Type II taste cells reside within the taste buds and are responsive to sweet, bitter, and umami, or savory, flavors.) Taste buds appeared smaller in the MRL/lpr mice than in the control mice. In tasting tests, the MRL/lpr mice showed decreased responsiveness to bitter, sweet, and umami flavors, but responded normally to salty and sour flavors. The research provides new evidence linking autoimmune disease and chronic inflammation to selective changes in the structure and function of taste tissues in the tongue. These findings offer opportunities for further explorations that have the potential to improve nutrition in people with chronic autoimmune disorders.

The poster "Defects in the Taste Structure and Function in MRL/lpr Autoimmune Disease Mice" (#41) takes place Thursday, April 14, 8:00 a.m. 12:00 p.m. ET in the Banyan Breezeway

The Sweet Taste of Anticipation

Before a flavor even hits the tongue, a subset of neurons in the gustatory cortex (GC), the area of the brain responsible for processing taste, is already primed to respond. These findings are based on experiments conducted by NIDCD-funded researcher Alfredo Fontanini, M.D., Ph.D., a 2010 Presidential Early Career Award for Scientists and Engineers (PECASE) winner. Matthew Gardner, a graduate student in Dr. Fontanini's laboratory, trained a group of rodents to self-administer a pulse of flavored water after hearing a flavor-specific tone. A sweet pulse would follow a "sweet" tone and a bitter pulse followed a "bitter" tone. Analysis of neuronal firing rates indicated that distinct subsets of GC neurons displayed patterns of unique activity that were specific to either the "sweet" or the "bitter" tone. To see how subsequent responses would be affected by misleading cues, the researchers followed the sweet tone with an unexpected pulse of bitter water. Looking at the GC, they saw that neurons were not as successful in discriminating between bitter and sweet as when the animals were properly cued. The neurons also took a longer amount of time to eventually exhibit bitter-specific activity. These findings suggest that neural responses in the GC aren't necessarily an accurate report of what is on the tongue and that the expectation of what one is about to taste elicits taste-specific activity in the GC that ultimately shapes the neural coding for taste.

The poster "Specific Expectation Modulates Taste Coding in Gustatory Cortex" (#43) takes place Thursday, April 14, 7:00 p.m. 11:00 p.m. ET in the Banyan Breezeway

Progression of Smell Loss Offers Clues to the Treatment of Alzheimer's Disease

Loss of smell is a characteristic early symptom among people with Alzheimer's disease, but the relationship between olfactory dysfunction and the progression of the disease is still relatively unknown. Daniel Wesson, Ph.D., will be presenting findings based on research funded by the NIDCD and conducted with colleagues at the Nathan S. Kline Institute for Psychiatric Research, the NYU School of Medicine, and Case Western Reserve School of Medicine. Their findings propose a pathological mechanism in the olfactory bulb, a small area of the brain above and behind the nose that transmits smell information to other areas of the brain for processing, could play a key role. Wesson and his colleagues used a mouse model that overexpresses a human mutation of amyloid precursor protein, a protein involved in making amyloid-beta (Aβ), which is the primary component of the plaques that form in the brains of Alzheimer's patients. When the mice were 3 months old, the researchers observed Aβ buildup in the olfactory bulb before accumulation in other brain areas and abnormal nervous hyperactivity within the olfactory bulb and the olfactory cortex, which receives input from the olfactory bulb. At 6 months of age, the mice showed impairment in their ability to smell. Later, at 16 months, as olfactory impairment persisted, and Aβ levels increased, the olfactory system became hypoactive. To directly test whether Aβ caused the dysfunction of olfactory behavior and neural activity, they administered a drug that helps break down Aβ. The drug reduced Aβ plaques by more than 50 percent in the olfactory system and other brain areas and also restored behavioral and neural olfactory function. Removing one olfactory bulb lowered the amount of Aβ found 6 months later on that side of the brain by more than 50 percent, even in regions that receive no direct olfactory bulb input. This supports a role for early-life olfactory bulb output in the spread of Aβ throughout the brain. These findings offer three potential applications: a new diagnostic marker that could help doctors diagnose Alzheimer's at earlier stages of the disease; a potential treatment to restore olfactory function in Alzheimer's patients; and a novel pathway for exploring drugs that could, ideally, slow or stop the progression of Alzheimer's disease. Other collaborators include: Anne H Borkowski, B.S., Gary E Landreth, Ph.D., Efrat Levy, Ph.D., Ralph A Nixon, M.D., Ph.D., and Donald A Wilson, Ph.D.

The platform presentation "Network dysfunction, olfactory behavior impairments, and their reversibility in an Alzheimer's β-amyloidosis mouse model" (#20) takes place Friday, April 15, at 9:45 a.m. ET in the Island Ballroom.


Contact: Robin Latham
NIH/National Institute on Deafness and Other Communication Disorders

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