Winnie Qian1, Tom A Schweizer2, Nathan W Churchill3, Colleen Millikin4, Zahinoor Ismail5, Eric E Smith5, Lisa M Lix6, David G Munoz7, Joseph J Barfett8, Tarek K Rajji9, Corinne E Fischer10. 1. Keenan Research Centre for Biomedical Research (WQ, TAS, NWC, DGM, JJB, CEF), Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto; the Institute of Medical Sciences (WQ, TAS, TKR, CEF), University of Toronto, Toronto. 2. Keenan Research Centre for Biomedical Research (WQ, TAS, NWC, DGM, JJB, CEF), Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto; the Institute of Medical Sciences (WQ, TAS, TKR, CEF), University of Toronto, Toronto; the Institute of Biomaterials and Biomedical Engineering (TAS), University of Toronto, Toronto; the Department of Surgery (TAS), Division of Neurosurgery, Faculty of Medicine, University of Toronto, Toronto; the Division of Neurosurgery (TAS), St. Michael's Hospital, Toronto. 3. Keenan Research Centre for Biomedical Research (WQ, TAS, NWC, DGM, JJB, CEF), Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto. 4. the Department of Clinical Healthy Psychology (CM), College of Medicine, Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada. 5. the Departments of Psychiatry and Neurology (ZI, EES), Mathison Centre for Mental Health Research & Education, Hotchkiss Brain Institute, University of Calgary, Calgary, Canada. 6. the Department of Community Health Sciences (LML), College of Medicine, University of Manitoba, Winnipeg, Canada. 7. Keenan Research Centre for Biomedical Research (WQ, TAS, NWC, DGM, JJB, CEF), Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto; the Department of Laboratory Medicine and Pathobiology (DGM), University of Toronto, Toronto; the Division of Pathology (DGM), St. Michael's Hospital, Toronto. 8. Keenan Research Centre for Biomedical Research (WQ, TAS, NWC, DGM, JJB, CEF), Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto; the Department of Medical Imaging (JJB), St. Michael's Hospital, Toronto. 9. the Institute of Medical Sciences (WQ, TAS, TKR, CEF), University of Toronto, Toronto; the Campbell Family Mental Health Research Institute (TKR), Centre for Addiction and Mental Health, Toronto; the Temerty Centre for Therapeutic Brain Intervention at the Centre for Addiction and Mental Health (TKR), Toronto. 10. Keenan Research Centre for Biomedical Research (WQ, TAS, NWC, DGM, JJB, CEF), Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto; the Institute of Medical Sciences (WQ, TAS, TKR, CEF), University of Toronto, Toronto; Department of Psychiatry (CEF), Faculty of Medicine, University of Toronto, Toronto. Electronic address: fischerc@smh.ca.
Abstract
OBJECTIVE: Delusions affect approximately a third of Alzheimer disease (AD) patients and are associated with poor outcomes. Previous studies investigating the neuroanatomic correlates of delusions have yet to reach a consensus, with findings of reduced volume across all lobes, particularly in frontal regions. The current study examined the gray matter (GM) differences associated with delusions in AD. METHODS: Using voxel-based morphometry, we assessed GM in 23 AD patients who developed delusions (AD+D) and 36 comparable AD patients who did not (AD-D) at baseline and follow-up. Analysis of variance was used to identify consistent differences between AD+D and AD-D patients across time points (main effect of group), consistent changes from baseline to follow-up (main effect of time), and differential changes between AD+D and AD-D over time (interaction of group and time). All data were obtained from the National Alzheimer's Coordinating Center database. RESULTS: The AD+D group had consistently lower frontal GM volume, although both groups showed decreased GM in frontotemporal brain regions over time. An interaction was observed between delusions and longitudinal change, with AD+D patients having significantly elevated GM in predominantly temporal areas at baseline assessment, becoming significantly lower than the AD-D group at follow-up. CONCLUSION: These findings suggest that, there are specific volumetric markers that distinguish patients with delusions from those without, before, and after the onset of delusions. Specifically, the decline of GM in temporal areas that had elevated levels prior to the onset of delusions may be involved in the manifestation of delusions.
OBJECTIVE: Delusions affect approximately a third of Alzheimer disease (AD) patients and are associated with poor outcomes. Previous studies investigating the neuroanatomic correlates of delusions have yet to reach a consensus, with findings of reduced volume across all lobes, particularly in frontal regions. The current study examined the gray matter (GM) differences associated with delusions in AD. METHODS: Using voxel-based morphometry, we assessed GM in 23 AD patients who developed delusions (AD+D) and 36 comparable AD patients who did not (AD-D) at baseline and follow-up. Analysis of variance was used to identify consistent differences between AD+D and AD-D patients across time points (main effect of group), consistent changes from baseline to follow-up (main effect of time), and differential changes between AD+D and AD-D over time (interaction of group and time). All data were obtained from the National Alzheimer's Coordinating Center database. RESULTS: The AD+D group had consistently lower frontal GM volume, although both groups showed decreased GM in frontotemporal brain regions over time. An interaction was observed between delusions and longitudinal change, with AD+D patients having significantly elevated GM in predominantly temporal areas at baseline assessment, becoming significantly lower than the AD-D group at follow-up. CONCLUSION: These findings suggest that, there are specific volumetric markers that distinguish patients with delusions from those without, before, and after the onset of delusions. Specifically, the decline of GM in temporal areas that had elevated levels prior to the onset of delusions may be involved in the manifestation of delusions.
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