Rebecca K West1, Abigail Livny2,3,4, Ramit Ravona-Springer3,4,5, Barbara B Bendlin6, Anthony Heymann4,7, Derek Leroith8, Xiaoyu Liu9, Hung-Mo Lin9, Hagit Hochner10, Yechiel Friedlander10, Ithamar Ganmore3,4,11, Amir Tirosh4,12, Michal Schnaider Beeri13,3. 1. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA. rebecca.west@mssm.edu. 2. Diagnostic Imaging Division, Sheba Medical Center, Ramat Gan, Israel. 3. The Joseph Sagol Neuroscience Center, Sheba Medical Center, Ramat Gan, Israel. 4. Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. 5. Psychiatric Division, Sheba Medical Center, Ramat Gan, Israel. 6. Department of Medicine, University of Wisconsin, Madison, WI, USA. 7. Maccabi Healthcare Services, Tel Aviv, Israel. 8. Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 9. Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 10. Braun School of Public Health, Hebrew University of Jerusalem, Jerusalem, Israel. 11. Department of Neurology, Sheba Medical Center, Ramat Gan, Israel. 12. Division of Endocrinology, Diabetes and Metabolism, Sheba Medical Center, Ramat Gan, Israel. 13. Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Abstract
AIMS/HYPOTHESIS: There are established relationships between adiposity (obesity) and higher dementia risk, faster cognitive decline and associated neural injury. Type 2 diabetes is strongly linked to greater adiposity and has been consistently associated with neural injury and poor cognitive outcomes. However, although obesity is a major cause of type 2 diabetes, there is limited evidence on the association of adiposity with brain atrophy among individuals with type 2 diabetes. METHODS: We examined the association of BMI (a measure of adiposity), and of long-term trajectories of BMI (three empirically identified groups of trajectories-'normal', 'overweight' and 'obese'-using SAS macro PROC TRAJ), with regional brain volume, in a sample of older individuals (aged 64-84) with type 2 diabetes participating in the Israel Diabetes and Cognitive Decline Study (n = 198). RESULTS: Using linear regression, we found that greater BMI was associated with smaller volumes of the inferior frontal gyrus (IFG) (r = -0.25, p = 0.001) and the middle temporal gyrus (r = -0.19; p = 0.010) after adjusting for sociodemographic covariates and total intracranial volume. In addition, there were significant differences between BMI trajectory groups in IFG volume (F = 4.34, p = 0.014), such that a long-term trajectory of obesity was associated with a smaller volume. Additional adjustment for cardiovascular and diabetes-related potential confounders did not substantively alter the results. There were no associations of adiposity with superior frontal gyrus, middle frontal gyrus or total grey matter volumes. CONCLUSIONS/ INTERPRETATION: In older adults with type 2 diabetes, long-term adiposity may have a detrimental impact on volume of brain regions relevant to cognitive functioning. Further studies to identify the underlying mechanisms are warranted. Graphical abstract.
AIMS/HYPOTHESIS: There are established relationships between adiposity (obesity) and higher dementia risk, faster cognitive decline and associated neural injury. Type 2 diabetes is strongly linked to greater adiposity and has been consistently associated with neural injury and poor cognitive outcomes. However, although obesity is a major cause of type 2 diabetes, there is limited evidence on the association of adiposity with brain atrophy among individuals with type 2 diabetes. METHODS: We examined the association of BMI (a measure of adiposity), and of long-term trajectories of BMI (three empirically identified groups of trajectories-'normal', 'overweight' and 'obese'-using SAS macro PROC TRAJ), with regional brain volume, in a sample of older individuals (aged 64-84) with type 2 diabetes participating in the Israel Diabetes and Cognitive Decline Study (n = 198). RESULTS: Using linear regression, we found that greater BMI was associated with smaller volumes of the inferior frontal gyrus (IFG) (r = -0.25, p = 0.001) and the middle temporal gyrus (r = -0.19; p = 0.010) after adjusting for sociodemographic covariates and total intracranial volume. In addition, there were significant differences between BMI trajectory groups in IFG volume (F = 4.34, p = 0.014), such that a long-term trajectory of obesity was associated with a smaller volume. Additional adjustment for cardiovascular and diabetes-related potential confounders did not substantively alter the results. There were no associations of adiposity with superior frontal gyrus, middle frontal gyrus or total grey matter volumes. CONCLUSIONS/ INTERPRETATION: In older adults with type 2 diabetes, long-term adiposity may have a detrimental impact on volume of brain regions relevant to cognitive functioning. Further studies to identify the underlying mechanisms are warranted. Graphical abstract.
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