Ph.D., Rutgers University, Psychobiology

Department of Psychology
Hunter College
695 Park Avenue
Room 631N
New York, NY 10065
Tel: (212) 772-5047
Fax: (212) 650-3647
Email: harding@genectr.hunter.cuny.edu

Current Areas of Research:

Behavioral Neuroimmunology:
Effects of mold exposure on immune activation, neuroplasticy, and behavior

I recently switched my research area from behavioral neuroendocrinology in birds to behavioral neuroimmunology in mice.  Over the last few years, evidence mounted that exposure to mold causes a broad range of health problems According to most estimates, about 33-40% of American buildings are moldy.  As a neuroscientist, I am particularly intrigued by the effects of mold exposure on neural function and cognition.  Recent research has documented that people who lived or worked in moldy buildings had multiple cognitive problems.  Compared to controls, mold-exposed individuals in one study scored below the 10th percentile on a number of cognitive tests. In other studies, mold-exposed patients demonstrated neurological deficits that correlated with their cognitive problems. Perhaps one of the most striking findings was that multiple studies concluded that individuals exposed to mold suffered cognitive deficits that could not be distinguished from those of patients suffering from mild traumatic brain injury. In addition, about 20% of Americans appear to be genetically-susceptible to long-term inflammation with resulting medical problems following mold exposure.

My current research seeks to develop a mouse model of the effects of mold exposure on neural and cognitive function. My basic hypothesis is that exposure to mold activates an immune response in the brain just as it does in peripheral tissues like the lungs. Prolonged immune activation is known to cause adverse neurological consequences. To date, we have documented that exposure to damp building molds causes hippocampal memory deficits, balance problems, and increased anxiety and fear.  These behavior problems are correlated with increased levels of activated immune cells in the hippocampus, increased levels of the proinflammatory cytokine interleukin 1b in the hippocampus, and decreases in two of three stages of neurogenesis.  Both toxic mold stimuli and skeletal elements common to all molds cause brain inflammation and behavioral problems.  We are just beginning to publish these results. 

Selected Publications:

Rauceo, S., Harding, C.F., Maldonado, A., Gaysinkaya, L., Tulloch, I. and Rodriguez, E. (2008) Dopaminergic modulation of reproductive behavior and activity in male zebra finches. Behavioural Brain Research, 187: 133-137 [PMID: 18160108]

Waterman, S.A. and Harding, C.F. (2008) Neurotoxic effects of DSP-4 on the central noradrenergic system, Behavioural Brain Research, 188: 271-280 [PMID: 18160108]Vyas, A., Harding, C.F., McGowan, J., Snare, R., and Bogdan, D. (2008) Noradrenergic neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSP-4), treatment eliminates estrogenic effects on song responsiveness in female zebra finches (Taeniopygia guttata).  Behav Neurosci. 122:1148-57. [PMID: 18823170].

Harding, C.F.  (2008) Hormonal modulation of singing behavior: Methodology and principles of hormone action.  In H.P. Zeigler and P. Marler (Eds.)  The Neuroscience of Birdsong: A Multidisciplinary Approach.  Cambridge: Cambridge University Press, pp. 305-319.

Vyas, A., Harding, C.F., Borg, L., and Bogdan, D. (2009) Acoustic characteristics, early experience, and endocrine status interact to modulate female zebra finches' behavioral responses to songs. Hormones and Behavior, 55: 50-59 [PMID: 18804474].