Ahmad Hariri
  • Ahmad Hariri

  • Professor of Psychology and Neuroscience
  • Psychology and Neuroscience
  • 417 Chapel Drive, 317 Soc/psyc, Durham, NC 27708
  • Campus Box 90086
  • Phone: (919) 681-8408
  • Homepage
  • Overview

    Integrating psychology, neuroimaging, pharmacology and molecular genetics in the search for biological pathways mediating individual differences in behavior and related risk for psychopathology.
  • Specialties

    • Cognition and Cognitive Neuroscience
    • Systems and Integrative Neuroscience
    • Clinical Psychology
  • Education

      • PhD,
      • Neuroscience,
      • UCLA,
      • 2001
      • Ph.D.,
      • University of California at Los Angeles,
      • 2000
      • M.S.,
      • University of Maryland, College Park,
      • 1997
      • B.S.,
      • University of Maryland, College Park,
      • 1994
  • Awards, Honors and Distinctions

      • Top 5% of all undergraduate instructors,
      • Unknown,
      • July, 2010
      • Distinguished Scientific Award for Early Career Contribution to Psychology,
      • APA,
      • January 2009
      • Distinguished Scientific Awards for Early Career Contributions to Psychology (individual differences),
      • American Psychological Association,
      • January 2009
  • Recent Publications

      • JL Hanson, AR Hariri and DE Williamson.
      • 2015.
      • Blunted Ventral Striatum Development in Adolescence Reflects Emotional Neglect and Predicts Depressive Symptoms.
      • Biological Psychiatry
      • 78:
      • 598-605
      • .
      • AR Hariri and A Holmes.
      • 2015.
      • Finding translation in stress research.
      • Nature Neuroscience
      • 18:
      • 1347-1352
      • .
      • NS Corral-Frías, YS Nikolova, LJ Michalski, DA Baranger, AR Hariri and R Bogdan.
      • 2015.
      • Stress-related anhedonia is associated with ventral striatum reactivity to reward and transdiagnostic psychiatric symptomatology..
      • Psychological medicine
      • 45:
      • 2605-2617
      • .
      Publication Description

      Early life stress (ELS) is consistently associated with increased risk for subsequent psychopathology. Individual differences in neural response to reward may confer vulnerability to stress-related psychopathology. Using data from the ongoing Duke Neurogenetics Study, the present study examined whether reward-related ventral striatum (VS) reactivity moderates the relationship between retrospectively reported ELS and anhedonic symptomatology. We further assessed whether individual differences in reward-related VS reactivity were associated with other depressive symptoms and problematic alcohol use via stress-related anhedonic symptoms and substance use-associated coping.Blood oxygen level-dependent functional magnetic resonance imaging (fMRI) was collected while participants (n = 906) completed a card-guessing task, which robustly elicits VS reactivity. ELS, anhedonic symptoms, other depressive symptoms, coping behavior, and alcohol use behavior were assessed with self-report questionnaires. Linear regressions were run to examine whether VS reactivity moderated the relationship between ELS and anhedonic symptoms. Structural equation models examined whether this moderation was indirectly associated with other depression symptoms and problematic alcohol use through its association with anhedonia.Analyses of data from 820 participants passing quality control procedures revealed that the VS × ELS interaction was associated with anhedonic symptoms (p = 0.011). Moreover, structural equation models indirectly linked this interaction to non-anhedonic depression symptoms and problematic alcohol use through anhedonic symptoms and substance-related coping.These findings suggest that reduced VS reactivity to reward is associated with increased risk for anhedonia in individuals exposed to ELS. Such stress-related anhedonia is further associated with other depressive symptoms and problematic alcohol use through substance-related coping.

      • MA Scult, JW Trampush, F Zheng, ED Conley, T Lencz, AK Malhotra, D Dickinson, DR Weinberger and AR Hariri.
      • 2015.
      • A Common Polymorphism inPredicts General Cognitive Ability through Effects on PFC Physiology.
      • Journal of Cognitive Neuroscience
      • 27:
      • 1766-1774
      • .
      • EC Nelson, A Agrawal, AC Heath, R Bogdan, R Sherva, B Zhang, R Al-Hasani, MR Bruchas, YL Chou, CH Demers, CE Carey, ED Conley, AK Fakira, LA Farrer, A Goate, S Gordon, AK Henders, V Hesselbrock, M Kapoor, MT Lynskey, PA Madden, JA Moron, JP Rice, NL Saccone, SG Schwab, FL Shand, AA Todorov, L Wallace, T Wang, NR Wray, X Zhou, L Degenhardt, NG Martin, AR Hariri, HR Kranzler, J Gelernter, LJ Bierut, DJ Clark and GW Montgomery.
      • 2015.
      • Evidence of CNIH3 involvement in opioid dependence..
      • Molecular psychiatry
      • .
      Publication Description

      Opioid dependence, a severe addictive disorder and major societal problem, has been demonstrated to be moderately heritable. We conducted a genome-wide association study in Comorbidity and Trauma Study data comparing opioid-dependent daily injectors (N=1167) with opioid misusers who never progressed to daily injection (N=161). The strongest associations, observed for CNIH3 single-nucleotide polymorphisms (SNPs), were confirmed in two independent samples, the Yale-Penn genetic studies of opioid, cocaine and alcohol dependence and the Study of Addiction: Genetics and Environment, which both contain non-dependent opioid misusers and opioid-dependent individuals. Meta-analyses found five genome-wide significant CNIH3 SNPs. The A allele of rs10799590, the most highly associated SNP, was robustly protective (P=4.30E-9; odds ratio 0.64 (95% confidence interval 0.55-0.74)). Epigenetic annotation predicts that this SNP is functional in fetal brain. Neuroimaging data from the Duke Neurogenetics Study (N=312) provide evidence of this SNP's in vivo functionality; rs10799590 A allele carriers displayed significantly greater right amygdala habituation to threat-related facial expressions, a phenotype associated with resilience to psychopathology. Computational genetic analyses of physical dependence on morphine across 23 mouse strains yielded significant correlations for haplotypes in CNIH3 and functionally related genes. These convergent findings support CNIH3 involvement in the pathophysiology of opioid dependence, complementing prior studies implicating the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate system.Molecular Psychiatry advance online publication, 4 August 2015; doi:10.1038/mp.2015.102.

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  • Postdoctoral Students

    • Johnna Swartz
      • 2013 - present
    • F Caroline Davis
      • 2012-2013
    • Fredrik Ahs
      • 2010-2013
    • Ryan Bogdan
      • 2010 - 2012
    • Justin Carre
      • 2010 - 2011
    • Jared Minkel
      • 2010 - 2011
    • Kristin McNealy
      • 2009 - 2011
  • Teaching

    • PSY 685S.01
      • BIOLOGICAL PATHWAYS
      • Soc/Psych 237
      • F 10:05 AM-01:00 PM