Francesca Filbey

Bert Moore Chair in BrainHealth
Professor - Behavioral and Brain Sciences
CBH 2.720
Filbey Lab
Tags: Cognition and Neuroscience

Professional Preparation

Postdoctoral Fellowship - Neuroimaging
National Institute of Mental Health, NIH - 2005
Doctor of Philosophy - Experimental Neuropsychology
Institute of Psychiatry, King's College, University of London - 2002
Master of Science - Applied Cognition and Neuroscience
University of Texas at Dallas - 1997
Bachelor of Arts - Psychology
University of Texas at Arlington - 1995

Research Areas

Research Interests:

In the United States, addictive disorders including substance use disorders and pathological overeating cause an extensive burden in terms of morbidity, mortality, and public health costs, yet treatment strategies are only modestly effective.  Better understanding of the biological mechanisms that underlie addictive disorders and increase susceptibility could substantially improve current prevention and intervention efforts. The overarching goal across my line of translational research is to characterize factors that increase risk for addictive disorders. Specifically, I am interested in how early life factors such as period of exposure (e.g., adolescent onset of regular use) or early life stress mediate the neural mechanisms that are associated with addictive disorders, and how genetic risk moderates these effects.

A translational neuroscience approach.The utility of combining genomic and neuroimaging approaches is becoming increasingly evident.  Neuroimaging provides a neurobiological phenotype that is proximal to the biological function of genetic variation.  Unlike other phenotypes, which may be affected by subjective factors, like reporter bias (e.g., in reporting subjective craving and/or the experience of addictive symptoms), neurobiological phenotypes are less influenced by other variables.  Using more objective phenotypes subsequently helps increase the power to detect the influence of the genetic variation.  In addition, neuroimaging provides a critical link between molecular changes and behavior, which also makes interpreting and translating the effects of genetic variation much more clear.  Over the last several years, I have developed a translational model that links changes at the neural level with changes at the behavioral level (Filbey, et al., 2008; Filbey, Slack, Sunderland, & Cohen, 2006; Filbey, Schacht, Myers, Chavez, & Hutchison, 2009b). The projects below describe how I have taken this approach to fill the knowledge gap on the biobehavioral mechanisms of addictive disorders.

Cue-reactivity in fMRI.  While there has been considerable controversy over the subjective “craving” in humans, the study of the biological mechanisms that underlie the positive reinforcing effects of stimuli in animals and humans has historically been much more straightforward. Previous studies have found that the motivation to use drugs is linked to the mesolimbic and mesocortical dopamine pathways in the brain and is an important factor in the etiology of addiction (Robinson & Berridge, 1993). Despite being less addictive than other substances of abuse, the published behavioral studies of marijuana suggest that craving is a reliable and valid phenomenon with this substance, analogous to craving for other drugs of abuse (e.g.,Haughey, Marshall, Schacht, Louis, & Hutchison, 2008). In the first neuroimaging study of cue-reactivity in marijuana users, I utilized a tactile cue paradigm (i.e., used marijuana pipe vs. pencil) in fMRI in marijuana users (Filbey et al., 2009b).  The imaging results showed that activity in the orbitofrontal cortex (OFC), anterior cingulate, amygdala, thalamus, insula, nucleus accumbens and ventral tegmental area (VTA) underlie cue-reactivity in marijuana, and that this pattern was positively correlated with marijuana-related problems.  This is notable, as it demonstrates that the areas of activation for marijuana are similar to other drugs of abuse such as cocaine, heroin, methamphetamine, alcohol, and tobacco (for review see Volkow et al., 2006).

In a more recent line of research, I have also been examining cue reactivity in tobacco dependent adults and binge eaters who meet criteria for obesity (BMI>30).  With tobacco smokers, I utilized video cues in an fMRI paradigm to elicit cue-elicited craving (Filbey et al, 2009). Specifically, I compared the BOLD response to smoking video clips with appetitive (e.g., food) video clips and found greater activation during the smoking cues in the bilateral anterior cingulate, right insula, and right superior and middle temporal gyri. Building upon this work, I have also evaluated the use of olfactory cues to determine the most potent modality in eliciting a stronger response within the reward system in smokers.  These analyses are underway.

Regarding obesity, researchers have suggested that aspects of disordered eating share mechanisms that have been previously implicated in addictions, specifically with respect to cue-elicited craving (Sheppard, 1993). People who pathologically overeat, such as binge eaters, report similar clinical symptoms to those that characterize substance addictions including craving, loss of control, impairment of functioning, preoccupation with the substance of choice (e.g., food), and the use of binge eating to regulate emotions and stress (Krahn & Gosnell, 1991). In this project, I examined fMRI BOLD response to food cues among individuals with obesity.  The fMRI paradigm consisted of gustatory presentations of the participant’s preferred high-caloric beverage (e.g., coca cola) and a control taste (i.e, water). When high-caloric beverage exposure was contrasted with water exposure, we found greater activation in several expected areas including the dorsal and ventral striatum, anterior cingulate, inferior frontal gyrus (IFG), and insula (Filbey, 2010).  These preliminary findings suggest a similar pattern of response for binge eaters as those with substance abuse disorders. 

Early life factors.  Early life stress has been found to negatively impact brain structure and function. In addition, studies have shown that the resultant neurobiological changes confer vulnerability for the development of brain disorders, specifically those related to stress such as substance abuse (Hayatbakhsh et al., 2008). However, despite clear links between early life stress and drug abuse, the neurobiological mechanisms that underlie this association remain unknown. We recently found that total score on the Early Life Stress Questionnaire was positively correlated with activation in the nucleus accumbens (NAc) during a cue exposure paradigm with heavy drinking adults. These findings suggest that exposure to early life stress is associated with increased neural response in an important area within the reward system during exposure to alcohol taste cues. This illustrates a possible mechanism by which early stress causes alterations in the dopaminergic system, which may subsequently increase one’s vulnerability to developing substance use disorders.

There is also growing literature suggesting that exposure to substances increases the brain’s sensitivity to their harmful effects. Contrary to the animal literature, the long-term effects of human adolescent substance abuse are not as clearly delineated. Studies have indicated that while other parts of the brain have matured by adolescence (areas controlling language, for example), cognitive control over high-risk behaviors is still maturing during adolescence, making teens more apt to engage in risky behaviors. Also, with the brain's emotion-related areas and connections still maturing, adolescents may additionally be more vulnerable to potential brain assaults that could impact the development of psychological disorders during this time.To examine this, we evaluated the role of early potential age of onset of marijuana use and fMRI BOLD response to marijuana cues.  The results showed a positive correlation between neural activation and age of onset (range = 9 – 22 years of age), such that the earlier the age of onset, the less the response to cues in the mid-frontal gyrus and anterior cingulate gyrus. These findings suggest that exposure to regular marijuana use at an early age (i.e., adolescence) leads to alterations in brain function, particularly in frontal executive control areas.

Genetic risk factors. Basic research on the human genome is progressing at a rapid pace. Twin and adoption studies have indicated that genetic variation accounts for approximately 50% of the variance in substance use disorders (for review see (Dick & Bierut, 2006). With regards to marijuana dependence, the psychoactive substance, cannabinoid-Δ9-tetrahydrocannabinol (THC), binds to central cannabinoid or CB1 receptors, which are widely distributed in the brain (Matsuda, Lolait, Brownstein, Young, & Bonner, 1990).  Subsequently, the logical candidate genes are those that regulate the cannabinoid system. I recently reported the first neuroimaging study of the genetic factors that impact the neurobiological processes in marijuana dependence. In this study, I examined the modulatory effects of both the cannabinoid receptor 1 (CNR1) and fatty acid amide hydrolase (FAAH) genotypes on neural response to marijuana cues. I found that the CNR1 and FAAH each moderated neural response to cues in reward areas of the brain, with an interactive effect between the two SNPs, such that the greater the number of risk alleles, the greater the neural response in reward areas (Filbey, Schacht, Myers, Chavez, & Hutchison, 2009a). In sum, these findings provide evidence for the strong influence of cannabinoid system modulating genes in moderating sensitivity to the effects of marijuana.  I plan to extend this work to my tobacco using and binge eating samples.

In conclusion,I believe that my research is important since the determination of intermediate phenotypes on the path to brain disorders such as addictive disorders is a necessity if we are to determine those at risk, develop treatments designed to prevent the development of the disease, and apply them safely, economically and expeditiously.


McDonald, C., Marshall, N., Sham, P.C., Bullmore, E.T. Schulze, K., Chapple, B., Bramon, E., Filbey, F. Quraishi, S., Walshe, M., Murray, R. (2006). Regional brain morphometry in patients with schizophrenia or bipolar disorder and their unaffected relatives, American Journal of Psychiatry, 163 (3), 478-487. 2006 - Publication
Kravariti, E., Toulopoulou, T., Mapua-Filbey, F., McDonald. C., Walshe, M., Sham, P., and Murray, R. (2006). Intellectual asymmetry and genetic liability in first-degree relatives of schizophrenia probands, British Journal of Psychiatry. 188, 186-187. 2006 - Publication
Filbey, F.M., Slack, K.J., Sunderland, T. and Cohen, R.M., (2005) Increased BOLD activity in midline frontal areas associated with apolipoprotein allele-?4 status in young healthy adults, NeuroImage, 26 (1). Presented in Human Brain Mapping, Toronto, Canada, June 12 – 16, 2005. 2005 - Publication
Dempster, E., Toulopoulou, T., McDonald, C., Bramon, E., Walshe, M., Filbey, F., Wickham, H., Sham, P. C., Murray, R. M., and Collier, D. A. (2005). Association between BDNF val(66) met genotype and episodic memory, Am J Med Genet B Neuropsychiatry Genet, 134(1), 73-75. 2005 - Publication
Filbey, F.M., Holroyd, T., Carver, F., Sunderland, T., and Cohen, R.M. (2005).  An MEG spatiotemporal analysis of neural activities during feature binding, NeuroReport. 16(16), 1747-1752. 2005 - Publication
Toulopoulou, T., Mapua-Filbey, F., Quraishi, S., Kravariti, E., Morris, R.G., McDonald, C., Walshe, M., and, Bramon, E., Murray, R. (2005). Cognitive performance in presumed obligate carriers for psychosis, British Journal of Psychiatry. 187, 284-285. 2005 - Publication
Bramon, E., McDonald, C., Croft, R.J., Landau, S., Filbey, F., Gruzelier, J.H., Sham, P.C., Frangou, S., and Murray, R.M. (2005). Is the P300 wave an endophenotype for schizophrenia? A meta-analysis and a family study, NeuroImage. 27(4), 960-968. 2005 - Publication
Filbey, F. M., Holroyd, T., Slack, K., Maltzman, L., Coppola, R., Sunderland, T., and Cohen, R. M. (2004). An MEG Study of the Spatiotemporal Dynamics of Feature Binding, Proceedings of the14th International Conference on Biomagnetism. 2004 - Publication
Mapua Filbey, F,Bayley, P.J. (2003). The 15th Annual Summer Institute in Cognitive Neuroscience in Review, NeuroImage 19 (2), 471-472 2003 - Publication
Mapua Filbey, F,Cohen, R, Sunderland, T (2002). Brain Imaging in Dementia.  In Handbook of Medical Psychiatry, Soares, JC and Gerson, S (eds.). New York: 497-520 2002 - Publication


Associate Professor
University of Texas at Dallas [2014–Present]
Assistant Professor
University of Texas at Dallas [2010–2014]
Assistant Professor of Translational Neuroscience
The Mind Research Network [2007–2010]
Honorary Researcher
Institute of Psychiatry [2007–Present]
Research Assistant Professor
University of New Mexico [2007–2010]
Research Assistant Professor
University of Colorado, Boulder [2005–2007]
Postdoctoral Fellowship
National Institute of Mental Health [2002–2005]
Research Assistant
Institute of Psychiatry University of London [1998–2000]
Research Assistant
Dallas Veterans Affairs Medical Center [1995–1998]

Additional Information

Pending Grant Applications as PI

1R01DA030344-01 “Genetic and environmental modulators of the brain’s response to marijuana cues”

  • NIH 5 years $2,062,750
  • Submitted February 2010 / Earliest start date: 12/1/2010

1DP2OD007082-01  “Using multivariate pattern recognition to predict vulnerability to substance abuse”

  • NIH 5 years $2,449,800
  • Submitted Oct 2009 / Earliest start date: 9/30/2010

1R01DK089105-01 “Imaging evidence for an overlapping neurocognitive model of obesity and drug addiction”         

  • NIH 5 years $2,686,862
  • Submitted Oct 2009 / Earliest start date: 9/30/2010

1RO1XXXXXXXX “(Sub-Award: Haughey) A Multi-Level Translational Approach to Medications Development for the Treatment of Cannabis-Related Disorders”

  • NIH 5 years $898,671
  • Submitted April 2010 / Earliest start date: 9/1/2010
Past Grant Funding
  • 2008 – 2009          MRN Transition Grant
                                     “Neurogenetic determinants of tobacco initiation and maintenance”
                                     Role: PI
  • 1999 - 2000           Margaret Temple Fellowship, British Medical Association
                                     “FMRI of attention in people with schizophrenia and their first-degree relatives”
                                     Role: PI
Personal Statement

My research interests are focused on combining neuroimaging and genetic techniques to characterize neural mechanisms associated with addictive disorders. Specifically, I am interested in how environmental factors (e.g., adolescent onset of use, early life stress) mediate the neural mechanisms that are associated with addictive disorders and how genetic risk moderates these effects. My current projects involve the determination of these effects using neuroimaging tools (sMRI, DTI, fMRI during resting state, cue-exposure tasks, reward and punishment tasks, response inhibition tasks and stress tasks) and a candidate gene approach in marijuana and tobacco users in addition to obese binge eaters.

News Articles

Consortium Studying Marijuana's Effects Receives $500,000 Grant
The National Institute on Drug Abuse (NIDA) has awarded a $500,000 grant to fund the Imaging Data in Emerging Adults with Addiction (IDEAA) Consortium — a large marijuana research data collection undertaking.

UT Dallas' Center for BrainHealth is partnering with Harvard University, the University of California, San Diego and the University of Wisconsin-Milwaukee to gain a greater scientific understanding of marijuana and its effects.
Center for BrainHealth Study Examines Marijuana's Long-Term Effects
The effects of chronic marijuana use on the brain may depend on when the user first consumed the drug and the duration of use, according to new research from the Center for BrainHealth at UT Dallas. 

In a paper published Monday in Proceedings of the National Academy of Sciences, researchers found that chronic marijuana users have smaller brain volume in the orbitofrontal cortex, which is commonly associated with addiction, and increased brain connectivity. It’s the first time researchers have described chronic users’ brain abnormalities with multiple magnetic resonance imaging (MRI) techniques. 
Habitual cannabis use alters brain oxygen
Dr. Francesca Filbey, the director of Cognitive Neuroscience Research in Addictive Disorders at the Center for BrainHealth at The University of Texas at Dallas, has recently led a new study analyzing the effects of tetrahydrocannabinol (THC), which is the main active substance in cannabis, on the brains of chronic cannabis users.

Tetrahydrocannabinol, the main active ingredient in cannabis, is linked to changes in how oxygen “travels” through the brain. This may correlate with changes in brain functions in the long-term, a new study argues.
Researcher Feels Driven to Understand Addiction
Addiction – to gambling, to alcohol, to food, to any compulsive human behavior without regard to consequences – can ruin lives.

Dr. Francesca Filbey, a new researcher in the Center for BrainHealth and an assistant professor in the School of Behavioral and Brain Sciences, is an expert on the subject who wants to learn still more. “I hope to be able to reveal the interactions between genetic and environmental factors that lead to addiction,” she said about her research.
Q&A with Dr. Francesca Filbe
How did you become interested in neuroscience?

When I was 12 years old my grandfather had a stroke. Since he lived with us, it was the first time I’d ever seen the impact of brain injury on a person’s life, so I decided to study psychology in college. My first job was doing schizophrenia research which quickly sparked my interest in the effects of genes and environment on brain health. I wanted to know how those two factors influence the brain. Using genetics and neuroimaging, I’ve looked at how genes and environment interact to lead to schizophrenia, Alzheimer’s, and addictive disorders.

Why study the brain, especially addiction?

There are a lot of reasons to study the brain. It’s important to look at how the normal brain functions in order to improve and maximize brain capacity and brain health and to also determine the mechanisms that lead to disorders.  Doing so could inform on how best to prevent and treat these disorders.  Here, at the Center for BrainHealth, I do research that evaluates how environmental and genetic contributions lead to brain changes that underlie addictive behavior.  The ultimate goal is to provide information towards the development of more targeted preventative and intervention strategies.


Current Memberships to Professional Societies

American College of Neuropsychopharmacology

College on Problems of Drug Dependence

Human Brain Mapping

Society for Neuroscience

Cognitive Neuroscience Society

Society for Behavioral Medicine

Research Society for Alcoholism