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

Honors & Awards

  • 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

Research & Scholarship

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

  • 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
  • Longitudinal investigation of neuroinflammation and metabolite profiles in the APPswe ×PS1?e9 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

    View details for DOI 10.1111/jnc.14251

  • 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

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