Christopher G. Janus, Ph.D.

Janus ChrisAssistant Professor

Department of Neuroscience
Center for Translational Research in Neurodegenerative Disease
Office Phone: (352) 273-9662


1978 M.S. Jagiellonian University, Cracow, Poland
1984 Ph.D. Polish Academy of Sciences and
Jagiellonian University, Cracow, Poland
1985-1986 Leverhulme Research Fellow Cambridge University, UK
1986-1987 Research Fellow King’s College, Cambridge University, UK
1988-1990 Postdoctoral Fellow Sub-Department of Animal Behaviour,
Cambridge University, UK

Key Words: Dementia, Neurodegenerative Disease

Research Focus & Aims:

Memory and ability to learn are the cognitive faculties that we as humans value most highly.  Age-associated neurodegenerative disorders compromise and eventually destroy our memory, “de-humanizing” (dementia) our lives.  The increase worldwide demographic aging is reflected by the increase in the number of people suffering from Alzheimer’s disease and related dementias.  Despite an enormous research effort, at present, there is no effective therapy for preventing or reducing the risks of developing dementia.  The clinically diagnosed symptoms of dementia are usually preceded by years or decades of slow progressing neuronal loss.  Also, the epidemiological studies indicate that certain amount of brain damage can be sustained before reaching the threshold of clinical identification, or that experience with cognitive tasks triggers compensatory mechanisms, which actively cope with the initial neural damage.  This apparent dissociation between the degree of brain damage and its clinical diagnosis limits the sensitivity of early diagnostic efforts. The identification of genes implicated in a number of neurodegenerative disorders has allowed for the development of animal models which not only replicate aspects of the human condition, but also simulate processes that occur in human brain, thus providing an insight into how disease is initiated and how it develops.

In our research, we use mouse models of neurodegenerative disorders to parse contributions of genetic and environmental factors, and their interactions on the onset and severity of dementia with underlying neuronal dysfunction and loss. These models might not only help us to understand the critical events and time-points of behavioral changes preceding dementia, but they might also help us to understand the mechanisms of memory formation and its retrieval. We focus on the development of cognitive impairment in these models, the behavioral plasticity leading to alternative strategies in solution of mnemonic tasks, and the environmental factors modulating such behaviors. A broader understanding of behavioral idiosyncrasies and abnormalities based on comprehensive evaluation of mouse behavioral phenotype will provide surrogate biomarker for the evaluation of non-pharmacological preventive strategies for these diseases, and will help to determine therapeutic efficacy of newly emerging treatments.

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