Volumetric and Shape Analysis of the Thalamus and Striatum in Amnestic Mild Cognitive Impairment

Article type: Research Article

Authors: Leh, Sandra E.^{a; *} | Kälin, Andrea M.^a | Schroeder, Clemens^a | Park, Min Tae M.^{b; c} | Chakravarty, M. Mallar^{b; d} | Freund, Patrick^{e; f; g; i} | Gietl, Anton F.^a | Riese, Florian^a | Kollias, Spyros^h | Hock, Christoph^a | Michels, Lars^{h; *}

Affiliations: [a] Division of Psychiatry Research and Psychogeriatric Medicine, University of Zurich, Switzerland | [b] Cerebral Imaging Centre, Douglas Mental Health University Institute, Montreal, Canada | [c] Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Canada | [d] Departments of Psychiatry and Biomedical Engineering, McGill University, Montreal, Canada | [e] Spinal Cord Injury Center, University Hospital Balgrist, Switzerland | [f] Department of Brain Repair and Rehabilitation, UCL Institute of Neurology, University College London, London, UK | [g] Wellcome Trust Centre for Neuroimaging, UCL Institute of Neurology, University College London, London, UK | [h] Institute of Neuroradiology, University of Zurich, Switzerland | [i] Department of Neurophysics, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany

Correspondence: [*] Correspondence to: Sandra E. Leh, Klinik für Alterspsychiatrie, Minervastrasse 145, CH-8032 Zurich, Switzerland. Tel.: +41 44 389 1652; E-mail: sandra.leh-seal@bli.uzh.ch

Correspondence: [*] Correspondence to: Lars Michels, University Hospital, Sternwartstr. 6, CH-8091 Zurich, Switzerland. Tel.: +41 44 255 4965; E-mail: lars.michels@usz.ch

Abstract: Alterations in brain structures, including progressive neurodegeneration, are a hallmark in patients with Alzheimer’s disease (AD). However, pathological mechanisms, such as the accumulation of amyloid and the proliferation of tau, are thought to begin years, even decades, before the initial clinical manifestations of AD. In this study, we compare the brain anatomy of amnestic mild cognitive impairment patients (aMCI, n = 16) to healthy subjects (CS, n = 22) using cortical thickness, subcortical volume, and shape analysis, which we believe to be complimentary to volumetric measures. We were able to replicate “classical” cortical thickness alterations in aMCI in the hippocampus, amygdala, putamen, insula, and inferior temporal regions. Additionally, aMCI showed significant thalamic and striatal shape differences. We observed higher global amyloid deposition in aMCI, a significant correlation between striatal displacement and global amyloid, and an inverse correlation between executive function and right-hemispheric thalamic displacement. In contrast, no volumetric differences were detected in thalamic, striatal, and hippocampal regions. Our results provide new evidence for early subcortical neuroanatomical changes in patients with aMCI, which are linked to cognitive abilities and amyloid deposition. Hence, shape analysis may aid in the identification of structural biomarkers for identifying individuals at highest risk of conversion to AD.

Keywords: Alzheimer’s disease, cortical thickness, hippocampus, mild cognitive impairment, shape analysis, striatum, thalamus, volumetry

DOI: 10.3233/JAD-150080

Journal: Journal of Alzheimer's Disease, vol. 49, no. 1, pp. 237-249, 2016