About

Christine DeLorenzo is an Associate Professor of Psychiatry and Biomedical Engineering at Stony Brook University. Her research focuses on biomarkers of Major Depressive Disorder, antidepressant treatment response prediction, and multimodal approaches to understanding mental health conditions. She is involved in exploring the intersection of biomedical engineering and psychiatry to develop predictive models and biomarkers that can improve diagnosis and treatment outcomes for depression.

Research topics

• Radiology
• Internal medicine
• Psychiatry
• Audiology
• Cardiology
• Psychology
• Medicine

Selected publications

• Obesity-related differences in amygdala and hippocampal volume and metabolism before and after a placebo-controlled antidepressant trial in major depressive disorder

  Scientific Reports · 2026-03-12

  articleOpen accessSenior author

  This study examined the association between obesity, measured by waist circumference (WC) and Body Mass Index (BMI), and neurobiology of the treatment/placebo response in depression. 85 participants (56 females, 29 males) with Major Depressive Disorder (MDD) were imaged using PET/MRI before and after a double-blind, randomized escitalopram trial. Analyses were pooled across interventions to investigate primary imaging associations. Linear mixed models examined associations between obesity measures and amygdala and hippocampal volume and metabolism. Preintervention obesity was significantly positively associated with amygdala and hippocampus volume, but not metabolism. Successful treatment is often associated with an increase in volume and a reduction in metabolism in these regions. However, greater WC and BMI were associated with decreases in amygdala volume following treatment/placebo. And greater BMI was associated with increases in amygdala and hippocampus metabolism following treatment/placebo. Importantly, however, these neurobiological changes were not associated with differential improvement in depression severity. Overall, this multimodal study shows obesity-related factors are associated with intervention-related neurobiological changes in MDD; however, additional research is needed to clarify whether these alterations correspond to meaningful variation in symptom improvement.

  PublisherOA PDFDOI

• Fatigue in major depression is linked to depression severity, not sleep duration or anterior cingulate cortex neurochemistry

  Journal of Affective Disorders · 2026-01-02 · 1 citations

  articleOpen accessSenior author

  In major depressive disorder (MDD), it is unclear whether fatigue is a result of poor sleep or depression, and its biological basis is unknown. To explore this, Magnetic Resonance Spectroscopy ( 1 H-MRS) in the anterior cingulate cortex (ACC) was acquired in unmedicated participants with MDD ( N = 76). Gamma-aminobutyric acid (GABA+) and Glx (combination of glutamate and glutamine) concentrations were quantified from an average co-edited difference spectrum, with preprocessing using Gannet and spectral fitting using TARQUIN. Participants (median age: 23.5 ± 14.2 years) completed sleep and depression questionnaires. The Wilcoxon rank sum or Kruskal-Wallis test was used to examine the marginal difference in continuous variables between levels of fatigue. Mediation effects of depression severity, GABA+, and Glx concentrations on the relationship between sleep duration and fatigue were evaluated using multivariable logistic regression models with fatigue as the dependent variable. Bayes Factor hypothesis testing examined the strength of evidence. Separate analyses were repeated with sleep efficiency as the main predictor. No significant relationship was observed between sleep duration/efficiency or GABA+/Glx and fatigue. Depression severity was significantly associated with fatigue and had a significant mediation effect on the relationship between sleep duration and fatigue. Specifically, for every additional hour of sleep, the odds of feeling fatigued nearly every day decreased by 11 % via an indirect mediating effect of decreased depression severity. GABA+/Glx did not mediate the effects of sleep on fatigue. The results suggest that, in this relatively young population, interventions to improve depression in MDD may be beneficial in reducing the debilitating effects of fatigue. • Sleep disturbances and fatigue are commonly reported in major depressive disorders (MDD). • However, it is unclear whether fatigue is solely a result of poor sleep or an independent symptom within MDD. • One way to disentangle these effects is to examine the levels of the primary neurotransmitters responsible for sleep and arousal, glutamate and γ-aminobutyric acid (GABA). • In this study, we examined the relationship between these neurotransmitters and sleep/fatigue in MDD. • Depression severity was significantly associated with fatigue and had a significant mediation effect on the relationship between sleep duration and fatigue. • Specifically, for every additional hour of sleep, the odds of feeling fatigued nearly every day decreased by 11 % via an indirect mediating effect of decreased depression severity.

  PublisherDOI

• Lack of association between pretreatment glutamate/GABA and major depressive disorder treatment response

  Translational Psychiatry · 2025-03-02 · 8 citations

  articleOpen accessSenior author

  Abstract Studies have shown gamma-amino-butyric acid (GABA) and Glx (a combination of glutamate and glutamine) to be altered in major depressive disorder (MDD). Using proton Magnetic Resonance Spectroscopy ( 1 H-MRS), this study aimed to determine whether lower pretreatment GABA and Glx levels in the medial frontal cortex, a region implicated in MDD pathophysiology, are associated with better antidepressant treatment response. Participants with MDD ( N = 74) were antidepressant naïve or medication-free for at least three weeks before imaging. Two MEGA-PRESS 1 H-MRS acquisitions were collected, interleaved with a water unsuppressed reference scan. GABA and Glx concentrations were quantified from an average difference spectrum, with preprocessing using Gannet and spectral fitting using TARQUIN. Following imaging, participants were randomized to escitalopram or placebo for 8 weeks in a double-blind design. Multivariable logistic regression models were applied with treatment type and age as covariates. Bayes Factor hypothesis testing was used to interpret the strength of the evidence. No significant association was found between pretreatment Glx, GABA, or Glx/GABA and depression remission status or the continuous outcome, percent change in symptom severity. In an exploratory analysis, no significant correlation was found between pretreatment Glx, GABA or Glx/GABA and days to response. Bayes factor analysis showed strong evidence towards the null hypotheses in all cases. To date, there are no replicated biomarkers in psychiatry. To address this, well-powered, placebo-controlled trials need to be undertaken and reported. The present analysis suggests pretreatment GABA, Glx, or their ratio cannot predict antidepressant treatment response. Future direction including examining glutamate and glutamine separately or examining biological subtypes of MDD separately. Trial Name: Advancing Personalized Antidepressant Treatment Using PET/MRI. Registration Number: NCT02623205 URL: https://clinicaltrials.gov/ct2/show/NCT02623205

  PublisherOA PDFDOI

• A central role for acetylcholine in entorhinal cortex function and dysfunction with age in humans and mice

  Cell Reports · 2025-01-30 · 4 citations

  articleOpen access

  Structural and functional changes in the entorhinal cortex (EC) are among the earliest signs of cognitive aging. Here, we ask whether a compromised cholinergic system influences early EC impairments and plays a primary role in EC cognition. We evaluated the relationship between loss of integrity of cholinergic inputs to the EC and cognitive deficits in otherwise healthy humans and mice. Using in vivo imaging (PET/MRI) in older humans and high-resolution imaging in wild-type mice and mice with genetic susceptibility to Alzheimer's disease pathology, we establish that loss of cholinergic input to the EC is, in fact, an early feature in cognitive aging. Through mechanistic studies in mice, we find a central role for EC-projecting cholinergic neurons in the expression of EC-related behaviors. Our data demonstrate that alterations to the cholinergic EC are an early, conserved feature of cognitive aging across species and may serve as an early predictor of cognitive status.

  PublisherDOI

• Obesity-Related Differences in Amygdala and Hippocampus Volume and Metabolism in Major Depressive Disorder: Implications for Antidepressant Treatment

  Research Square · 2025-05-08

  preprintOpen accessSenior author
  PublisherOA PDFDOI

• Quantifying Ventricular CSF Clearance in the Human Brain Using Dynamic 18F-FDG PET: Insights into Age-Related Glymphatic Impairment

  medRxiv · 2025-04-09 · 4 citations

  preprintOpen access

  Abstract Purpose The glymphatic system facilitates brain waste clearance via cerebrospinal fluid (CSF) flow, and its dysfunction has been linked to aging and neurodegeneration. However, clinically accessible methods to quantify glymphatic function in humans remain limited. This study aimed to examine the potential of dynamic 18F-FDG PET for measuring ventricular CSF clearance - as a surrogate marker of glymphatic function. Specifically, we evaluated its association with age, its test–retest reliability, and the feasibility of reduced scan durations for clinical applicability. Methods We analyzed 72 baseline 18F-FDG PET scans from participants enrolled in a prior depression trial. Time–activity curves (TACs) were extracted from the lateral ventricles and fitted with a γ-variate model to estimate influx ( μ in ) and clearance ( μ out ) parameters. Associations with age and clinical factors were examined using correlation and multiple linear regression. Test–retest reliability was assessed in 11 placebo-treated participants who underwent repeat scans eight weeks apart. A feasibility analysis tested whether shorter scan windows could yield comparable clearance estimates. Results μ out showed a strong negative correlation with age (r = –0.680, p < 0.001), while μ in was not significantly age-related. Age remained a significant predictor of μ out after adjusting for sex, ventricle size, and depression severity. A positive association between μ out and depression severity was observed after covariate adjustment. Test–retest analysis yielded an intraclass correlation coefficient of 0.702 for μ out , indicating moderate-to-good reproducibility. A shortened 30-minute scan window (starting 30 minutes post injection) preserved strong correlations with both μ out and age, supporting the potential for abbreviated imaging protocols. Conclusion Dynamic 18F-FDG PET provides a reliable and noninvasive method to quantify ventricular CSF clearance, revealing age-related decline indicative of glymphatic impairment. The method demonstrates reproducibility over time and retains key clearance metrics even with shortened scan durations. These findings establish a clinically feasible 18F-FDG PET-based approach for studying brain clearance and glymphatic function in aging and disease.

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• Abstract 4358270: Sodium-Glucose Cotransporter-2 Inhibitor Use Is Associated with Improved Cognitive Outcomes in Older Heart Failure Patients: A Comparative Analysis Using Real-World Clinical Data

  Circulation · 2025-11-03

  article

  Background: Cognitive impairment is a frequent and debilitating comorbidity in older adults with heart failure (HF). Sodium-glucose cotransporter-2 inhibitors (SGLT2i) improve HF-related outcomes, but their effect on cognitive outcomes is not well established. Research Question: Does treatment with the SGLT2i empagliflozin or dapagliflozin reduce the incidence of cognitive impairment in older adults with HF? Methods: We conducted a retrospective, propensity score-matched cohort study using TriNetX, a global electronic health records database. Adults ≥60 years of age with a diagnosis of HF between July 1, 2020, and March 31, 2023, were included ( Figure 1 ). Patients with pre-existing dementia, type 1 diabetes or chronic kidney disease were excluded. A total of 50,188 SGLT2i users (empagliflozin n=32,761 [65.3%]; dapagliflozin n=17,427 [34.7%]) were propensity score–matched 1:1 to non-user controls based on demographic and clinical variables. Outcomes were assessed over a 2-year follow-up, and included incident diagnosis of Alzheimer’s disease (AD), vascular dementia (VD), mild cognitive impairment (MCI), unspecified dementia, and drugs related to AD. Cox proportional hazards models were used to estimate hazard ratios (HRs). Results: The matched cohorts had a mean age of 72.0 years (empagliflozin) and 71.5 years (dapagliflozin); approximately 58–59% were male and 43–49% had diabetes mellitus. Baseline characteristics were adequately matched ( Table 1 ). Empagliflozin use was associated with significantly reduced risk of AD (HR 0.61, 95% CI 0.48–0.77, p<0.001), VD (HR 0.56, 95% CI 0.44–0.71, p<0.001), unspecified dementia (HR 0.59, 95% CI 0.52–0.67, p<0.001), and initiation of drugs related to AD (HR 0.73, 95% CI 0.62–0.85, p<0.001) ( Table 2 ) Dapagliflozin showed similar protective associations with VD (HR 0.48, 95% CI 0.33–0.68, p<0.001), unspecified dementia (HR 0.65, 95% CI 0.54–0.77, p<0.001), initiation of drugs related to AD (HR 0.76, 95% CI 0.61–0.96, p=0.021), and MCI (HR 0.76, 95% CI 0.60–0.97, p=0.028). Conclusion: In a real-world study of older adults with heart failure, empagliflozin and dapagliflozin use was associated with a lower risk of incident cognitive impairment. While mechanisms such as improved cerebral perfusion, attenuation of neuroinflammation or modulation of metabolic and vascular pathways implicated in neurodegeneration are plausible, prospective studies are needed to confirm these associations and elucidate causal pathways.

  PublisherDOI

• Connecting the dots: approaching a standardized nomenclature for molecular connectivity in positron emission tomography

  European Journal of Nuclear Medicine and Molecular Imaging · 2025-06-02 · 10 citations

  reviewOpen access

  Abstract Positron emission tomography (PET)-based connectivity analysis provides a molecular perspective that complements fMRI-derived functional connectivity. However, lack of standardized terminology and diverse methodologies in PET connectivity studies has resulted in inconsistencies, complicating the interpretation and comparison of results across studies. A standardized nomenclature is thus needed to reduce ambiguity, enhance reproducibility, and facilitate interpretability across radiotracers, imaging modalities and studies. Here, we define and differentiate the terms “molecular connectivity” and “molecular covariance”. Drawing parallels from other imaging modalities, we propose “molecular connectivity” as an umbrella term to characterize statistical dependencies between the measured PET signal across brain regions at a within-subject level. Like fMRI resting-state functional connectivity, “molecular connectivity” leverages spatio-temporal associations in the PET signal to derive brain network associations. Conversely, “molecular covariance” denotes group-level computations of covariance matrices between-subjects . Further specification of the terminology can be achieved by including the target of the employed radioligand, such as “metabolic connectivity/covariance” for [ 18 F]FDG or “amyloid covariance” for [ 18 F]flutemetamol and “tau covariance” for [ 18 F]flortaucipir. While this approach to standardization aims to clarify terminology, open questions remain about the neurobiological underpinnings of these connectivity metrics. Future research should focus on elucidating these mechanisms and developing advanced computational methodologies that evaluate diverse feature relationships and improve the robustness of PET-based connectivity metrics.

  PublisherOA PDFDOI

• Glial activation among individuals with neurological post-acute sequelae of coronavirus disease 2019: A positron emission tomography study of brain fog using [18F]-FEPPA

  Brain Behavior & Immunity - Health · 2025-01-18 · 3 citations

  articleOpen access

  This study examined the regional distribution of glial activation in essential workers with neurological post-acute sequelae of coronavirus disease 2019 (COVID-19) infections (N-PASC). We injected ≤185 MBq of [ 18 F]-FEPPA as an intravenous bolus and positron-emission tomography over 2 h. To measure distribution volume (V T ) we recruited 24 essential workers (14 N-PASC, 10 Never-COVID-19 Controls, of whom 22 successfully placed arterial lines). Individuals with low binding affinity were excluded from this study, and V T was adjusted for translocator protein genotype. Analyses that passed the false discovery rate are reported. Participants at midlife survived mild to moderate COVID-19 without hospitalization but reported onset of post-acute sequelae of COVID-19 (PASC) for, on average, 22 months before undergoing neuroimaging. Hippocampal V T was higher (V T = 1.70, 95% C.I. = [1.30–2.21], p = 0.001) in participants with persistent brain fog after COVID-19, reflecting an increase of 10.58 mL/cm 3 in V T (area under the receiver-operating curve, AUC = 0.95 [0.85–1.00]). At a cutoff of 10.6, sensitivity/specificity/accuracy were 0.88/0.93/0.91. The results from this study imply that neuroimmune response is a distinct and identifiable characteristic of brain fog after COVID-19. Results suggest that [ 18 F]-FEPPA could be used to support N-PASC diagnosis. • Neurological symptoms are a central feature of post-acute sequelae of COVID-19. • To date, there are no protocols for monitoring brain health in PASC. • Glial activation on positron-emission tomography achieved excellent accuracy. • At a cutoff of 10.6, sensitivity/specificity/accuracy were 0.88/0.93/0.91.

  PublisherDOI

• Data-driven imaging marker for cerebral consequences of Post-Acute Sequelae of COVID19 - prospective validation and [18F]FEPPA PET correlation

  Proceedings on CD-ROM - International Society for Magnetic Resonance in Medicine. Scientific Meeting and Exhibition/Proceedings of the International Society for Magnetic Resonance in Medicine, Scientific Meeting and Exhibition · 2025-09-16

  article

  Motivation: Recognizing neurological symptoms in Post-Acute Sequelae of COVID-19 (PASC), this study investigates neuroinflammatory markers to develop reliable neuroimaging diagnostics. Goal(s): To validate CoreFA, a data-driven imaging marker, for detecting white matter changes and to explore its correlation with [18F]FEPPA PET neuroinflammatory markers. Approach: Diffusion MRI-derived fractional anisotropy (FA) was assessed in white matter tracts to derive CoreFA. CoreFA was validated in a prospective cohort and examined for association with neuroinflammation via FEPPA PET. Results: CoreFA demonstrated high diagnostic accuracy (AUC = 0.81 for initial group; AUC = 0.77 for prospective cohort). [18F]FEPPA PET scans confirmed neuroinflammation in regions with reduced FA. Impact: The strong correlation between CoreFA and neuroinflammatory markers from PET imaging provides a potential biomarker for assessing PASC-related brain changes.

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Recent grants

• NIH Grant K01MH091354

  NIH · $691k · 2015

• NIH Grant R01MH104512

  NIH · $2.9M · 2020

Frequent coauthors

• Ramin V. Parsey

  Stony Brook Medicine

  181 shared

• John Gardus

  Stony Brook Medicine

  71 shared

• Chuan Huang

  61 shared

• J. John Mann

  New York State Psychiatric Institute

  50 shared

• Kathryn Hill

  Stony Brook Medicine

  48 shared

• Mala Ananth

  National Institute of Neurological Disorders and Stroke

  41 shared

• Elizabeth Bartlett

  Columbia University

  40 shared

• María A. Oquendo

  University of Pennsylvania

  40 shared

Education

• PhD, Biomedical Engineering

  Yale University

  2007

• MS, Biomedical Engineering

  Dartmouth College

  2001

• AB, Engineering

  Dartmouth College

  1999