Neuroimaging biologist with extensive experience in clinical and preclinical multimodal molecular imaging techniques within the field of psychiatric and neurodegenerative disease research.

Honors & Awards

  • ERF-SNMMI Postdoctoral Molecular Imaging Scholar Program Grant, Education and Research Foundation for Nuclear Medicine and Molecular Imaging (2018-2020)
  • Institute of Population Health Postgraduate showcase prize, individual center winner, Centre of Imaging Sciences, University of Manchester (2016)
  • Bio-Imaging Institute fully funded PhD scholarship, University of Manchester (2012-2016)
  • Biotechnology and Biological Sciences Research Council fully funded MRes scholarship, BBSRC (2011-2012)

Boards, Advisory Committees, Professional Organizations

  • Founder, MIPS/Canary trainee council, Stanford University (2017 - Present)
  • Member of the women in molecular imaging network (WIMIN) and WIMIN leadership trainee sub-committee, World Molecular Imaging Society (WMIS) (2017 - Present)
  • Member and participant in mentorship program, Association for Women in Science (AWIS) (2017 - Present)
  • Member, Women in Bio (WIB) (2017 - Present)
  • Member, European Society of Molecular Imaging (ESMI) (2012 - 2016)
  • Member, British Neuroscience Association (BNA) (2011 - 2016)

Professional Education

  • Doctor of Philosophy, University of Manchester (2016)
  • Master of Science, Imperial College of Science, Technology & Medicine (2012)
  • Bachelor of Arts, University Of Dublin, Trinity College (2011)

Stanford Advisors

Current Research and Scholarly Interests

Research Focus:
Developing and evaluating imaging techniques to enhance understanding and diagnosis of neurological disorders. My current research focuses on imaging neuroinflammation in neurodegenerative disorders such as stroke, Alzheimer's disease and multiple sclerosis using positron emission tomography (PET) and magnetic resonance (MR) techniques.
My previous research topics include investigating the effects of childhood maltreatment and major depressive disorder on brain morphology.

Neurobiology, neuroimaging, PET imaging, MRS/MRI, neuroinflammation, pre-clinical cognitive assessments, cell culture, science communication.

Lab Affiliations

All Publications

  • Infection Augments Expression of Mechanosensing Piezo1 Channels in Amyloid Plaque-Reactive Astrocytes FRONTIERS IN AGING NEUROSCIENCE Velasco-Estevez, M., Mampay, M., Boutin, N., Chaney, A., Warn, P., Sharp, A., Burgess, E., Moeendarbary, E., Dev, K. K., Sheridan, G. K. 2018; 10
  • PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke JoVE Chaney, A., Johnson, E. M., Cropper, H. C., James, M. L. 2018

    View details for DOI 10.3791/57243

  • 11C-DPA-713 versus 18F-GE-180: A preclinical comparison of TSPO-PET tracers to visualize acute and chronic neuroinflammation in a mouse model of ischemic stroke. Journal of nuclear medicine : official publication, Society of Nuclear Medicine Chaney, A., Cropper, H. C., Johnson, E. M., Lechtenberg, K. J., Peterson, T. C., Stevens, M. Y., Buckwalter, M. S., James, M. L. 2018


    Neuroinflammation plays a key role in neuronal injury following ischemic stroke. Positron emission tomography (PET) imaging of translocator protein 18 kDa (TSPO) permits longitudinal, non-invasive visualization of neuroinflammation in both pre-clinical and clinical settings. Many TSPO tracers have been developed, however it is unclear which tracer is the most sensitive and accurate for monitoring the in vivo spatiotemporal dynamics of neuroinflammation across applications. Hence, there is a need for head-to-head comparisons of promising TSPO-PET tracers across different disease states. Accordingly, the aim of this study was to directly compare two promising second-generation TSPO tracers; 11C-DPA-713 and 18F-GE-180, for the first time at acute and chronic time-points following ischemic stroke. Methods: Following distal middle cerebral artery occlusion (dMCAO) or sham surgery, mice underwent consecutive PET/CT imaging with 11C-DPA-713 and 18F-GE-180 at 2, 6, and 28 days after stroke. T2-weighted magnetic resonance (MR) images were acquired to enable delineation of ipsilateral (infarct) and contralateral brain regions of interest (ROIs). PET images were analyzed by calculating % injected dose per gram (%ID/g) in MR-guided ROIs. Standardized uptake value ratios were determined using the contralateral thalamus as a pseudo-reference region (SUVTh). Ex vivo autoradiography and immunohistochemistry were performed to verify in vivo findings. Results: Significantly increased tracer uptake was observed in the ipsilateral compared to contralateral ROI (SUVTh, 50-60 min summed data) at acute and chronic time-points using 11C-DPA-713 and 18F-GE-180. Ex vivo autoradiography confirmed in vivo findings demonstrating increased TSPO-tracer uptake in infarcted versus contralateral brain tissue. Importantly, a significant correlation was identified between microglial/macrophage activation (CD68 immunostaining) and 11C-DPA-713-PET signal, that was not evident with 18F-GE-180. No significant correlations were observed between TSPO-PET and activated astrocytes (GFAP immunostaining). Conclusion: Both 11C-DPA-713 and 18F-GE-180-PET enable detection of neuroinflammation at early and chronic time-points following cerebral ischemia in mice. 11C-DPA-713-PET reflects the extent of microglial activation in infarcted dMCAO mouse brain tissue more accurately compared to 18F-GE-180, and appears to be slightly more sensitive. These results highlight the potential of 11C-DPA-713 for tracking microglial activation in vivo after stroke, and warrants further investigation in both pre-clinical and clinical settings.

    View details for DOI 10.2967/jnumed.118.209155

    View details for PubMedID 29976695

  • Longitudinal investigation of neuroinflammation and metabolite profiles in the APPswe ×PS1Δe9 transgenic mouse model of Alzheimer's disease J Neurochem Chaney, A., Bauer, M., Bochicchio, D., Smigova, A., Kassiou, M., Davies, K. E., Williams, S. R., Boutin, H. 2017: 318–35


    There is increasing evidence linking neuroinflammation to many neurological disorders including Alzheimer's disease (AD); however, its exact contribution to disease manifestation and/or progression is poorly understood. Therefore, there is a need to investigate neuroinflammation in both health and disease. Here, we investigate cognitive decline, neuroinflammatory and other pathophysiological changes in the APPswe ×PS1Δe9 transgenic mouse model of AD. Transgenic (TG) mice were compared to C57BL/6 wild type (WT) mice at 6, 12 and 18 months of age. Neuroinflammation was investigated by [18 F]DPA-714 positron emission tomography and myo-inositol levels using 1 H magnetic resonance spectroscopy (MRS) in vivo. Neuronal and cellular dysfunction was investigated by looking at N-acetylaspartate (NAA), choline-containing compounds, taurine and glutamate also using MRS. Cognitive decline was first observed at 12 m of age in the TG mice as assessed by working memory tests . A significant increase in [18 F]DPA-714 uptake was seen in the hippocampus and cortex of 18 m-old TG mice when compared to age-matched WT mice and 6 m-old TG mice. No overall effect of gene was seen on metabolite levels; however, a significant reduction in NAA was observed in 18 m-old TG mice when compared to WT. In addition, age resulted in a decrease in glutamate and an increase in choline levels. Therefore, we can conclude that increased neuroinflammation and cognitive decline are observed in TG animals, whereas NAA alterations occurring with age are exacerbated in the TG mice. These results support the role of neuroinflammation and metabolite alteration in AD and in ageing.

    View details for DOI 10.1111/jnc.14251

    View details for PubMedCentralID PMC5846890

  • Effect of childhood maltreatment on brain structure in adult patients with major depressive disorder and healthy participants JOURNAL OF PSYCHIATRY & NEUROSCIENCE Chaney, A., Carballedo, A., Amico, F., Fagan, A., Skokauskas, N., Meaney, J., Frodl, T. 2014; 39 (1): 50-59


    Childhood maltreatment has been found to play a crucial role in the development of psychiatric disorders. However, whether childhood maltreatment is associated with structural brain changes described for major depressive disorder (MDD) is still a matter of debate. The aim of this study was to investigate whether patients with MDD and a history of childhood maltreatment display more structural changes than patients without childhood maltreatment or healthy controls.Patients with MDD and healthy controls with and without childhood maltreatment experience were investigated using high-resolution magnetic resonance imaging (MRI), and data were analyzed using voxel-based morphometry.We studied 37 patients with MDD and 46 controls. Grey matter volume was significantly decreased in the hippocampus and significantly increased in the dorsomedial prefrontal cortex (DMPFC) and the orbitofrontal cortex (OFC) in participants who had experienced childhood maltreatment compared with those who had not. Patients displayed smaller left OFC and left DMPFC volumes than controls. No significant difference in hippocampal volume was evident between patients with MDD and healthy controls. In regression analyses, despite effects from depression, age and sex on the DMPFC, OFC and hippocampus, childhood maltreatment was found to independently affect these regions.The retrospective assessment of childhood maltreatment; the natural problem that patients experienced more childhood maltreatment than controls; and the restrictions, owing to sample size, to investigating higher order interactions among factors are discussed as limitations.These results suggest that early childhood maltreatment is associated with brain structural changes irrespective of sex, age and a history of depression.Thus, the study highlights the importance of childhood maltreatment when investigating brain structures.

    View details for DOI 10.1503/jpn.120208

    View details for Web of Science ID 000336276300008

    View details for PubMedID 23900024

    View details for PubMedCentralID PMC3868665

  • Neural correlates of treatment outcome in major depression INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY Lisiecka, D., Meisenzahl, E., Scheuerecker, J., Schoepf, V., Whitty, P., Chaney, A., Moeller, H., Wiesmann, M., Frodl, T. 2011; 14 (4): 521-534


    There is a need to identify clinically useful biomarkers in major depressive disorder (MDD). In this context the functional connectivity of the orbitofrontal cortex (OFC) to other areas of the affect regulation circuit is of interest. The aim of this study was to identify neural changes during antidepressant treatment and correlates associated with the treatment outcome. In an exploratory analysis it was investigated whether functional connectivity measures moderated a response to mirtazapine and venlafaxine. Twenty-three drug-free patients with MDD were recruited from the Department of Psychiatry and Psychotherapy of the Ludwig-Maximilians University in Munich. The patients were subjected to a 4-wk randomized clinical trial with two common antidepressants, venlafaxine or mirtazapine. Functional connectivity of the OFC, derived from functional magnetic resonance imaging with an emotional face-matching task, was measured before and after the trial. Higher OFC connectivity with the left motor areas and the OFC regions prior to the trial characterized responders (p<0.05, false discovery rate). The treatment non-responders were characterized by higher OFC-cerebellum connectivity. The strength of response was positively correlated with functional coupling between left OFC and the caudate nuclei and thalami. Differences in longitudinal changes were detected between venlafaxine and mirtazapine treatment in the motor areas, cerebellum, cingulate gyrus and angular gyrus. These results indicate that OFC functional connectivity might be useful as a marker for therapy response to mirtazapine and venlafaxine and to reconstruct the differences in their mechanism of action.

    View details for DOI 10.1017/S1461145710001513

    View details for Web of Science ID 000289374500007

    View details for PubMedID 21205435