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Research Grants 2012


To view an abstract, select an author from the vertical list on the left.

2012 Grants - Llano

Diminished Cortical GABAergic Inhibition in a Mouse Model of Alzheimer's Disease

Daniel Llano, M.D., Ph.D.
University of Illinois at Urbana-Champaign
Urbana, Illinois

2012 New Investigator Research Grant

A growing number of studies suggest that brain cells become overly excited in Alzheimer's disease. This toxic process, known as excitotoxicity, often occurs when levels of a neurotransmitter (or chemical messenger) called glutamate become overproduced. Too much glutamate may overstimulate neurons and the synapses (or tiny channels) through which brain cells communicate. This pathology can lead to cognitive loss and brain cell death. Another neurotransmitter that may be involved in excitotoxicity is gamma-aminoburytic acid (GABA). GABA normally helps prevent neurons from becoming overexcited, but this function appears to decline in Alzheimer's disease. Loss of GABA function affects specific "circuitry" in the brain—pathways through which neurons in various brain regions send chemical signals to one another. The most affected pathways are likely the corticocortical system (which connects cells within the cerebral cortex) and the thalamocortical system (which connects cells between the cerebral cortex and the thalamus). Yet scientists know little about how these circuits are damaged by GABA dysfunction and excitotoxicity.

Daniel Llano, M.D., Ph.D., and colleagues plan to study GABA-induced circuitry problems using mice engineered to develop Alzheimer's-like symptoms. They will assess how the animals' corticocortical system and thalamocortical system may become "desensitized" to the protective effects of GABA. They will then try to identify particular neurons in the mice brains that are damaged by the loss of GABA function. For these efforts, the researchers will use novel optical and imaging techniques. Results of their work could shed new light on how neurotransmitter changes in Alzheimer's affect brain cell communication and cognitive loss.