Sean M Nestor1, Bratislav Mišić2, Joel Ramirez3, Jiali Zhao4, Simon J Graham5, Nicolaas P L G Verhoeff6, Donald T Stuss7, Mario Masellis8, Sandra E Black9. 1. LC Campbell Cognitive Neurology Research Unit, Ontario, Canada; Heart and Stroke Foundation Canadian Partnership for Stroke Recovery, Ontario, Canada; Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada; Institute of Medical Science, University of Toronto, Ontario, Canada; MD/PhD Program, Faculty of Medicine, University of Toronto, Ontario, Canada. Electronic address: sean.nestor@mail.utoronto.ca. 2. Department of Psychological and Brain Sciences, Indiana University, IN, USA. 3. LC Campbell Cognitive Neurology Research Unit, Ontario, Canada; Heart and Stroke Foundation Canadian Partnership for Stroke Recovery, Ontario, Canada; Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada. 4. LC Campbell Cognitive Neurology Research Unit, Ontario, Canada; Heart and Stroke Foundation Canadian Partnership for Stroke Recovery, Ontario, Canada. 5. Heart and Stroke Foundation Canadian Partnership for Stroke Recovery, Ontario, Canada; Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada; Department of Medical Biophysics, University of Toronto, Ontario, Canada. 6. Department of Psychiatry, Baycrest Health Sciences Centre and University of Toronto, Ontario, Canada. 7. Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada; Department of Medicine, University of Toronto, Ontario, Canada; Department of Psychology, University of Toronto, Ontario, Canada; Rotman Research Institute, Baycrest Health Sciences Centre, Ontario, Canada. 8. LC Campbell Cognitive Neurology Research Unit, Ontario, Canada; Heart and Stroke Foundation Canadian Partnership for Stroke Recovery, Ontario, Canada; Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada; Institute of Medical Science, University of Toronto, Ontario, Canada; Department of Medicine, Neurology, Sunnybrook Health Sciences Centre, University of Toronto, Ontario, Canada. 9. LC Campbell Cognitive Neurology Research Unit, Ontario, Canada; Heart and Stroke Foundation Canadian Partnership for Stroke Recovery, Ontario, Canada; Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada; Institute of Medical Science, University of Toronto, Ontario, Canada; Rotman Research Institute, Baycrest Health Sciences Centre, Ontario, Canada; Department of Medicine, Neurology, Sunnybrook Health Sciences Centre, University of Toronto, Ontario, Canada; Ontario Brain Institute, Ontario, Canada.
Abstract
INTRODUCTION: Cerebral small vessel disease (SVD) is thought to contribute to Alzheimer's disease (AD) through abnormalities in white matter networks. Gray matter (GM) hub covariance networks share only partial overlap with white matter connectivity, and their relationship with SVD has not been examined in AD. METHODS: We developed a multivariate analytical pipeline to elucidate the cortical GM thickness systems that covary with major network hubs and assessed whether SVD and neurodegenerative pathologic markers were associated with attenuated covariance network integrity in mild AD and normal elderly control subjects. RESULTS: SVD burden was associated with reduced posterior cingulate corticocortical GM network integrity and subneocorticocortical hub network integrity in AD. DISCUSSION: These findings provide evidence that SVD is linked to the selective disruption of cortical hub GM networks in AD brains and point to the need to consider GM hub covariance networks when assessing network disruption in mixed disease.
INTRODUCTION:Cerebral small vessel disease (SVD) is thought to contribute to Alzheimer's disease (AD) through abnormalities in white matter networks. Gray matter (GM) hub covariance networks share only partial overlap with white matter connectivity, and their relationship with SVD has not been examined in AD. METHODS: We developed a multivariate analytical pipeline to elucidate the cortical GM thickness systems that covary with major network hubs and assessed whether SVD and neurodegenerative pathologic markers were associated with attenuated covariance network integrity in mild AD and normal elderly control subjects. RESULTS:SVD burden was associated with reduced posterior cingulate corticocortical GM network integrity and subneocorticocortical hub network integrity in AD. DISCUSSION: These findings provide evidence that SVD is linked to the selective disruption of cortical hub GM networks in AD brains and point to the need to consider GM hub covariance networks when assessing network disruption in mixed disease.
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