Bio

Bio


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

Honors & Awards


  • Young investigator of the year award winner, World molecular imaging society (WMIS)/world molecular imaging congress (WMIC) (2019)
  • Women in Molecular Imaging Network (WIMIN) scholar award, World Molecular Imaging Society (WMIS)/world molecular imaging congress (WMIC) (2019)
  • Student travel stipend award, World Molecular Imaging Society (WMIS)/world molecular imaging congress (WMIC) (2019)
  • Best oral presentation, Stanford Neuroscience Forum (2019)
  • ERF-SNMMI Postdoctoral Molecular Imaging Scholar Program Grant, Education and Research Foundation for Nuclear Medicine and Molecular Imaging-SNMMI (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


  • Member, Radiology Diversity Committee, Stamford (2018 - Present)
  • 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.

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

Lab Affiliations


Publications

All Publications


  • 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

    Abstract

    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 PubMedID 29976695

  • Longitudinal investigation of neuroinflammation and metabolite profiles in the APPswe ÎPS1?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: 318?35

    Abstract

    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 ÎPS1?e9 transgenic mouse model of AD. Transgenic (TG) mice were compared to C57BL/6 wild type (WT) mice at 6, 12 and 18ámonths of age. Neuroinflammation was investigated by [18 F]DPA-714 positron emission tomography and myo-inositol levels using 1 H magnetic resonance spectroscopy (MRS) inávivo. 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 12ám 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 18ám-old TG mice when compared to age-matched WT mice and 6ám-old TG mice. No overall effect of gene was seen on metabolite levels; however, a significant reduction in NAA was observed in 18ám-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

  • Longitudinal TSPO-PET imaging of peripheral and central myeloid cells in a mouse model of complex regional pain syndrome. Pain Cropper, H. C., Johnson, E. M., Haight, E., Cordonnier, S. A., Chaney, A. M., Forman, T. E., Biswal, A., Stevens, M. Y., James, M. L., Tawfik, V. L. 2019

    Abstract

    Complex regional pain syndrome (CRPS) is a severely disabling disease characterized by pain, temperature changes, motor dysfunction and edema that most often occurs as an atypical response to a minor surgery or fracture. Inflammation involving activation and recruitment of innate immune cells, including both peripheral and central myeloid cells (i.e. macrophages and microglia, respectively), is a key feature of CRPS. However, the exact role and time-course of these cellular processes relative to the known acute and chronic phases of the disease are not fully understood. Positron emission tomography (PET) of translocator protein-18kDa (TSPO) is a method for non-invasively tracking these activated innate immune cells. Here, we reveal the temporal dynamics of peripheral and central inflammatory responses over 20 weeks in a tibial fracture/casting mouse model of CRPS through longitudinal TSPO-PET using [F]GE-180. PET tracer uptake quantification in the tibia revealed increased peripheral inflammation as early as 2 days post-fracture and lasting 7 weeks. Centralized inflammation was detected in the spinal cord and brain of fractured mice at 7 and 21 days post-injury. Spinal cord tissue immunofluorescent staining revealed TSPO expression in microglia (CD11b+) at 7 days, but was restricted mainly to endothelial cells (PECAM1+) at baseline and 7 weeks. Our data suggest early and persistent peripheral myeloid cell activation, and transient central microglial activation are limited to the acute phase of CRPS. Moreover, we show that TSPO-PET can be used to noninvasively monitor the spatiotemporal dynamics of myeloid cell activation in CRPS progression with potential to inform disease phase-specific therapeutics.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

    View details for PubMedID 31095093

  • 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. Journal of visualized experiments : JoVE Chaney, A. M., Johnson, E. M., Cropper, H. C., James, M. L. 2018

    Abstract

    Neuroinflammation is central to the pathological cascade following ischemic stroke. Non-invasive molecular imaging methods have the potential to provide critical insights into the temporal dynamics and role of certain neuroimmune interactions in stroke. Specifically, Positron Emission Tomography (PET) imaging of translocator protein 18 kDa (TSPO), a marker of activated microglia and peripheral myeloid-lineage cells, provides a means to detect and track neuroinflammation in vivo. Here, we present a method to accurately quantify neuroinflammation using [11C]N,N-Diethyl-2-[2-(4-methoxyphenyl)-5,7-dimethylpyrazolo[1,5-a]pyrimidin-3-yl]acetamide ([11C]DPA-713), a promising second generation TSPO-PET radiotracer, in distal middle cerebral artery occlusion (dMCAO) compared to sham-operated mice. MRI was performed 2 days post-dMCAO surgery to confirm stroke and define the infarct location and volume. PET/Computed Tomography (CT) imaging was carried out 6 days post-dMCAO to capture the peak increase in TSPO levels following stroke. Quantitation of PET images was conducted to assess the uptake of [11C]DPA-713 in the brain and spleen of dMCAO and sham mice to assess central and peripheral levels of inflammation. In vivo [11C]DPA-713 brain uptake was confirmed using ex vivo autoradiography.

    View details for PubMedID 29985311

  • In vivo molecular imaging of neuroinflammation in Alzheimer's disease. Journal of neurochemistry Chaney, A., Williams, S. R., Boutin, H. 2018

    Abstract

    It has become increasingly evident that neuroinflammation plays a critical role in the pathophysiology of Alzheimer's disease (AD) and other neurodegenerative disorders. Increased glial cell activation is consistently reported in both rodent models of AD and in AD patients. Moreover, recent genome wide association studies have revealed multiple genes associated with inflammation and immunity are significantly associated with an increased risk of AD development (e.g. TREM2). Non-invasive inávivo detection and tracking of neuroinflammation is necessary to enhance our understanding of the contribution of neuroinflammation to the initiation and progression of AD. Importantly, accurate methods of quantifying neuroinflammation may aid early diagnosis and serve as an output for therapeutic monitoring and disease management. This review details current inávivo imaging biomarkers of neuroinflammation being explored and summarizes both pre-clinical and clinical results from molecular imaging studies investigating the role of neuroinflammation in AD, with a focus on positron emission tomography and magnetic resonance spectroscopy (MRS).

    View details for DOI 10.1111/jnc.14615

    View details for PubMedID 30339715

  • 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

    Abstract

    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

    Abstract

    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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