Department of Neurosciences
Case Western Reserve University
School of Medicine
How does the brain integrate environmental information in order to guide behavioral responses? How and why does this process become impaired in cases of neurological disorders (i.e.., Alzheimer's disease) and normal aging? Addressing these questions is a critical step in not only understanding normal brain function, but also, to understand mechanisms of disease action and thus therapeutic strategies.
A major area of research within the lab is determining the role of the olfactory tubercle (OT) in olfactory processing. The OT is a prominent part of the basal forebrain and, despite being described as early as the mid 19th century, very little is know regarding its role in processing odors. Does the olfactory tubercle play a critical and unique role in olfactory perception? We are exploring this by using acute and awake-behaving electrophysiological methods in mice performing olfactory tasks. Related, we are also interested in understanding the mechanisms of olfactory-auditory integration in the olfactory cortex, including the OT. In both of these projects we employ molecular-genetic and chemical methods to silence or activate defined populations of cells to aid in determining precise mechanics of cell-cell communication. Finally, we are exploring the occurrence, nature, and sensory influences which determine the active sampling of odors within social interactions to provide novel insights into not only olfactory system function but also the neurobiology of social behaviors.
We are also keenly applying our skills to understanding how information processing becomes impaired during cases of neurodegeneration. Using transgenic mouse models of Alzheimer’s disease, we have developed a model of clinically-relevant cognitive dysfunction centered around changes in olfactory perception. In this model, behavior is sensitive to even minimal levels of amyloid-beta deposition, as is olfactory bulb and piriform cortex activity – 2 centers essential in the processing of odors. Taking advantage of this system, we are exploring methods to modulate levels of pathogenic features, including amyloid-beta but also other aspects related to amyloid precursor protein (APP) processing, to understand the mechanisms of sensory loss in Alzheimer’s disease. Importantly, by tapping into system neuroscience methods, we are able to record from neural ensembles in behaving animals to assay the influence of AD pathogenesis on complex stimulus-driven behaviors – something not possible in other physiological models in the field.
Together these two unique lines of research compliment an understanding of information processing in the brain in a translational manner.
PLEASE VISIT THE LAB WEBPAGE FOR MORE INFORMATION [http://wessonlab.blogspot.com/].