Amanda L Elton
· Assistant ProfessorVerifiedUniversity of Florida · Psychiatry and Behavioral Sciences
Active 2012–2026
About
Amanda L Elton, Ph.D., is an Assistant Professor in the Department of Psychiatry at the University of Florida College of Medicine. She received her undergraduate degree in neuroscience from The College of William and Mary, a master's degree in pharmacology from Emory University, and a Ph.D. in clinical and translational sciences from the University of Arkansas for Medical Sciences. Her scientific training continued at the University of North Carolina at Chapel Hill, where she was awarded a K01 research career development award from NIAAA to study the neural correlates of risk for alcohol use disorder. Dr. Elton's research interests include elucidating the effects of early life stress, heritable risk, and substance use on neurocognitive processes relevant for addiction and other psychopathologies, utilizing neuroimaging and behavioral methods. Her work focuses on neurocognitive aspects of addiction such as discounting of delayed rewards, response inhibition, sustained attention, and attentional bias towards rewards and drug cues. She applies innovative functional neuroimaging techniques to examine how activity and connectivity of brain networks support addiction-related behaviors, aiming to inform treatment and prevention strategies. Her recent research includes longitudinal studies on the neurocognitive mechanisms of risk and resilience for alcohol use disorder, with particular attention to early life stress and genetic factors, as well as sex differences. Dr. Elton also investigates neurocognitive markers of addiction risk using large datasets like the ABCD study, and her work involves combining neuroimaging, behavioral, and pharmacological approaches to better understand addiction vulnerability and resilience.
Research topics
- Neuroscience
- Psychology
- Biology
- Cognitive psychology
Selected publications
Benzodiazepines at the crossroads: navigating therapeutic promise and perils of misuse
Annals of General Psychiatry · 2026-02-02 · 1 citations
articleOpen accessSenior authorBenzodiazepines (BZDs) are a widely prescribed class of psychoactive drugs known for their rapid anxiolytic, anticonvulsant, and sedative effects. Introduced as safer alternatives to barbiturates, BZDs quickly gained popularity across clinical settings but have since become a subject of public health concern due to rising rates of misuse, dependence, and overdose, particularly when co-administered with opioids. This narrative review explores the historical development, pharmacologic mechanisms, clinical indications, and adverse outcomes associated with BZD use, while highlighting emerging areas of research such as pharmacogenetics (PGx) and genome-wide association studies (GWAS). BZDs act as positive allosteric modulators of the GABAA receptor, enhancing inhibitory neurotransmission. This mechanism underlies both their therapeutic efficacy and their potential for physiological dependence and misuse. Clinical applications span acute anxiety, insomnia, seizure management, and alcohol withdrawal; however, long-term use carries significant risks including cognitive decline, fall-related injuries, paradoxical excitation, and withdrawal syndromes. Reinforcement and neuroadaptation processes within the mesolimbic dopamine system contribute to BZD addiction, especially with chronic exposure. Regulatory responses include Schedule IV classification under the Controlled Substances Act and FDA black box warnings. Despite declining prescription rates in recent years, misuse, including nonmedical use and use of illicit designer BZDs, remains prevalent, especially among older adults and those with comorbid psychiatric or substance use disorders. Pharmacogenomic studies have identified genetic polymorphisms in hepatic enzymes (e.g., Cyp2c19 and Cyp3a4) and GABAA receptor subunits (e.g. Gabra2) that may influence BZD metabolism, efficacy, and addiction vulnerability, suggesting potential for personalized medicine approaches. In conclusion, the dual nature of BZDs, as essential tools in acute care and potential contributors to substance use disorders, demands a balanced, evidence-informed approach. Continued research, improved prescriber education, and integration of genetic insights into clinical care may help mitigate harm while preserving therapeutic benefit.
UNC Libraries · 2026-03-25
articleOpen accessAlcohol Clinical and Experimental Research · 2026-04-01
articleOpen access1st authorCorrespondingINTRODUCTION: A family history of alcohol use disorder (AUD) is associated with increased personal risk for alcohol misuse and AUD. Family history of AUD is also related to increased impulsivity as measured by delay discounting tasks, representing a potential mechanistic link between family history and alcohol misuse. Delay discounting tasks assess individual differences in preferences for smaller, immediate versus larger, delayed rewards, the former being linked to substance misuse. Decision-making on such tasks is underpinned by multiple neural systems, including those supporting reward valuation, cognitive control, and future-oriented thinking. We hypothesized that family history of AUD would be associated with differences in one or more neural systems related to delay discounting, with differences relating to increases in alcohol misuse in young adulthood. METHODS: We tested 163 first-year college students (105 females, ages 18-19) with varying levels of familial risk for AUD on a functional magnetic resonance imaging (fMRI) delay discounting task. Alcohol misuse was self-reported at baseline and in 3-yearly follow-up surveys using the Alcohol Use Disorders Identification Test (AUDIT). Change in alcohol misuse was modeled using a latent growth model, and we examined mediation between family history and alcohol misuse trajectory (AUDIT intercept and slope) through functional activation of brain regions implicated in reward valuation (nucleus accumbens), cognitive control (middle frontal gyrus), and future-oriented thinking (hippocampus). RESULTS: Family history of AUD was associated with greater nucleus accumbens activation (β = 0.286, SE = 0.117, p = 0.014), which in turn predicted a steeper AUDIT slope (β = 0.513, SE = 0.162, p = 0.002). No other mediators were significant. DISCUSSION: Our results demonstrate that nucleus accumbens function may be a key mechanism by which family history increases risk for alcohol misuse and AUD.
Journal of the American Academy of Child & Adolescent Psychiatry · 2025-04-11 · 5 citations
articleOpen accessSenior authormedRxiv · 2025-09-04
preprintOpen access1st authorCorrespondingA family history (FH) of alcohol use disorder (AUD) is associated with increased personal risk for alcohol misuse and AUD. FH is also related to increased impulsivity as evidenced by performance on delay discounting tasks, representing a potential mechanistic link between FH and alcohol misuse. Delay discounting tasks assess individual differences in preferences for smaller, immediate versus larger, delayed rewards, the former being linked to substance misuse. Decision-making on such tasks is underpinned by multiple neural systems, including those supporting reward valuation, cognitive control, and future-oriented thinking. We hypothesized that FH would be associated with differences in one or more neural systems related to delay discounting, with these differences being related to increases in alcohol misuse in young adulthood. We tested 163 first-year college students (ages 18-19) with varying levels of familial risk for AUD on an fMRI delay discounting task. Alcohol misuse was self-reported at baseline and in three yearly follow-up surveys using the Alcohol Use Disorders Identification Test (AUDIT). Alcohol misuse was modeled using a latent growth model, and we examined mediation between FH and alcohol misuse trajectory (AUDIT intercept and slope) through functional activation of brain regions implicated in reward valuation (nucleus accumbens), cognitive control (middle frontal gyrus), and future-oriented thinking (hippocampus). FH was associated with greater activation of the nucleus accumbens, which in turn predicted a steeper AUDIT slope. No other mediators were significant. Our results demonstrate that nucleus accumbens function may be a key mechanism by which FH increases risk for alcohol misuse and AUD.
An investigation of multimodal predictors of adolescent alcohol initiation
Drug and Alcohol Dependence · 2024-11-01 · 7 citations
articleOpen accessAddictive Behaviors · 2024-01-04 · 7 citations
articleOpen accessAIM: While the United States is becoming increasingly Multiracial, much is still unknown about the behavioral health of these growing new generations of Multiracial Americans. To narrow this research gap, this study investigated the prevalence/frequency of substance use and major depressive episodes [MDE] among non-Hispanic Multiracial [NHM] adolescents compared to their non-Hispanic White [NHW] counterparts and whether racial differences vary by socioeconomic status. METHODS: We analyzed data from the 2015-2019 National Survey on Drug Use and Health (N = 3,645 NHM and 34,776 NHW adolescents aged 12-17). Average Marginal Effects derived from logistic regression and negative binomial regression were used to examine (1) differences in six outcomes (past-month use of alcohol, cannabis, or drugs other than cannabis [DOTC], past-year MDE, and the frequency of alcohol and cannabis use among past-month users) by Multiracial status; (2) the moderation effect of family income on these associations. RESULTS: Compared to high-income NHW adolescents, high-income NHM adolescents reported significantly higher prevalence of past-month cannabis and DOTC use, and past-year MDE. No racial differences were observed at other income levels. Furthermore, moderation analyses indicated that the effect of Multiracial status on MDE was larger in the highest income group compared to the lowest income group. CONCLUSION: Our findings suggested that NHM adolescents, particularly those from high income families, exhibit increased prevalence of drug use and depression than NHW adolescents. As the US becomes more diverse, there is a need to further examine the social and structural factors driving the identified racial differences.
UNC Libraries · 2024-07-27
articleOpen accessBehavioral flexibility, the ability to modify behavior according to changing conditions, is essential to optimize decision-making. Deficits in behavioral flexibility that persist into adulthood are one consequence of adolescent alcohol exposure, and another is decreased functional connectivity in brain structures involved in decision-making; however, a link between these two outcomes has not been established. We assessed effects of adolescent alcohol and sex on both Pavlovian and instrumental behaviors and resting-state functional connectivity MRI in adult animals to determine associations between behavioral flexibility and resting-state functional connectivity. Alcohol exposure impaired attentional set reversals and decreased functional connectivity among cortical and subcortical regions-of-interest that underlie flexible behavior. Moreover, mediation analyses indicated that adolescent alcohol-induced reductions in functional connectivity within a subnetwork of affected brain regions statistically mediated errors committed during reversal learning. These results provide a novel link between persistent reductions in brain functional connectivity and deficits in behavioral flexibility resulting from adolescent alcohol exposure.
Molecular Psychiatry · 2024-11-22 · 3 citations
articleOpen access1st authorCorrespondingDrug and Alcohol Dependence · 2024-07-01
article
Recent grants
The neural mechanisms of risk for alcohol use disorder among college students
NIH · $308k · 2022–2024
Frequent coauthors
- 43 shared
Charlotte A. Boettiger
University of North Carolina at Chapel Hill
- 20 shared
Wei Gao
Cedars-Sinai Medical Center
- 14 shared
Sarael Alcauter
Universidad Nacional Autónoma de México
- 10 shared
Clinton D. Kilts
University of Arkansas for Medical Sciences
- 9 shared
Woomi Ban
- 9 shared
Yen‐Yu Ian Shih
- 9 shared
Donita L. Robinson
- 9 shared
Sung‐Ho Lee
Louisiana State University in Shreveport
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