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About Us

Photo of EEG electrodes and subject cap

CNL-R is a group of scientists, clinicians, and technicians based in the University of Rochester Medical Center Department of Neuroscience. We’re interested in understanding how the brain processes input from our sense organs. We have a particular interest in how conditions and disorders with genetic and neurological components affect sensory perception and sense-related cognition. To date, researchers in our lab have published articles related to Autism Spectrum Disorder, Dyslexia, Multiple Sclerosis, Neimann Pick Type C, addiction, ADHD, and Rett Syndrome, to name a few. Current research foci include Batten Disease, Rett Syndrome, dyslexia, neurological complications of AIDS, and sex differences in Autism.

We utilize a variety of techniques including electroencephalography, electrocorticography, functional magnetic resonance imaging, and transgenic murine models to study the characteristics of these diseases and how they are manifested in the brain. Our mission is to identify and understand the physiology of the fundamental deficits behind these syndromes and to connect these deficiencies to common genetic, physiological, and behavioral traits. Furthering our knowledge of these diseases has allowed us to develop clinical trials to ameliorate these deficits and definitively measure that progress.

We began operation at the University of Rochester School of Medicine and Dentistry in the beginning of 2016 and our lab will soon take up residence on the top floor of the Rochester Center for Brain Imaging, located across the street from the URMC’s School of Medicine and Dentistry.

The Lab can be contacted via or (585) 275-1674.
If you are interested in participating as a subject in any of our studies, please see the listings in the Help Wanted panel.

Multisensory Integration

Image of active regions of brains in fMRI

Multisensory processing occurs very early, both in terms of the anatomical and temporal processing hierarchies. The functional significance of early interactions in sensory cortical areas is not well understood. Recent work has shown that cortical integration mechanisms are highly malleable and adaptable and appear to affected by task parameters, contextual setting, and cognitive factors.

The current project is directed at unpacking the functional significance of the brain processes associated with multisensory integration. We're interrogating a three-stage temporal model of cortical multisensory processing that provides an elementary framework for our investigations. It represents a crucial step in the parsing of the principles of cortical multisensory processing.


Locations of brain regions active in task

Electrocorticography (ECoG) is a neuroimaging technique that places specially designed electrodes directly on the surface of the cortex that are capable of recording the microvoltage potentials generated by populations of discharging neurons. It registers neuronal activity instantaneously, giving it high temporal resolution. Furthermore, because the dura mater, skull and scalp are not present to impede and diffuse the electrical signals of firing neurons, it yields high spatial resolution with high sensitivity. As such, ECoG provides a powerful amount of information in the hands of researchers who investigate how discrete sensory systems, each with spatially discrete populations of dedicated neurons, coordinate to perform the tasks that predicate phenotypic behavior. Our lab collaborates with URMC’s Epilepsy Department to make this unique and incredibly valuable research possible.


Image representing stimuli used in testing of Dyslexia

Dyslexia, the failure to develop appropriate reading proficiency despite adequate opportunity and intact hearing and vision, affects between 5-17% of the population. Why do individuals who learn well in myriad other domains, and are often of high intelligence, struggle so with this particular task?

Long before confronting the task of learning to read, infants and toddlers form cross-sensory associations between the sensory representations of complex real-world objects - the sound of a running faucet, the meow of the family cat, the clapping of a mother’s hands. Work by our group and others has shown that when only one sensory representation of such objects is presented to an observer, there is an automatic co-activation of the contra-sensory representation. In dyslexia, this automatic co-activation appears fundamentally broken for the written word. But what of other object classes, presumably acquired much earlier in development? Do these children acquire automatic multisensory object representations for common non-linguistic environmental objects, or are these also ‘multisensorially’ impoverished’? If so, this would suggest that a more fundamental deficit in multisensory object encoding predates their issues with reading.

Lysosomal Storage Disorders

Contour maps of heads representing Rhett syndrom

Rett Syndrome is a rare genetic neurological disorder typically caused by a de novo mutation of the MECP2 gene. Early in childhood development, Rett syndrome steals the ability to speak alongside the presentation of a wide range of motor and social impairments. This inability to communicate is a profound hindrance to normal development and happiness.

Children with Batten disease experience progressive cognitive and behavioral decline. Progression of cognitive deficits involves impairments of attention, working memory, language, and global declines in intellect. Deficits in verbal attention and memory span are noted early in the disease course, and have also been documented in presymptomatic children.

Our lab is currently working on research that employs our electrophysiological techniques to assess the cognitive capacity of children afflicted with these diseases to produce markers of disease decline and, when therapies are developed, disease recovery.

Inhibitory Control of HIV+ Abstinent Cocaine Users

MRI Image and Plot gragh from HIV+ subjects

Combined HIV+ serostatus and cocaine use poses a serious personal and public health risk. Cocaine accelerates the transition from HIV+ to AIDS1, possibly due to reduced HIV medication adherence in substance-abusing individuals2. In addition, HIV- individuals who currently abuse cocaine frequently practice high-risk sexual behaviors such as inconsistent condom usage.

However, it is unknown whether risky decision-making in the cohort of HIV+ individuals with a history of drug dependence continues after prolonged drug abstinence. Furthermore, while recent research on former cocaine users suggests normalization of electrophysiological responses associated with inhibitory control6, it is unknown whether this recovery trajectory persists in the presence of HIV.

This study seeks to understand the neural and behavioral markers associated with risky decision-making in HIV+ individuals with a history of cocaine dependence.