Eelco van Duinkerken1, Menno M Schoonheim2, Martijn D Steenwijk3, Martin Klein4, Richard G IJzerman5, Annette C Moll6, Martijn W Heymans7, Frank J Snoek4, Frederik Barkhof3, Michaela Diamant5. 1. Diabetes Center/Department of Internal Medicine, VU University Medical Center, Amsterdam, the Netherlands Department of Medical Psychology, VU University Medical Center, Amsterdam, the Netherlands e.vanduinkerken@vumc.nl. 2. Department of Radiology and Nuclear Medicine, VU University Medical Center, Amsterdam, the Netherlands Department of Anatomy and Neuroscience, VU University Medical Center, Amsterdam, the Netherlands. 3. Department of Radiology and Nuclear Medicine, VU University Medical Center, Amsterdam, the Netherlands. 4. Department of Medical Psychology, VU University Medical Center, Amsterdam, the Netherlands. 5. Diabetes Center/Department of Internal Medicine, VU University Medical Center, Amsterdam, the Netherlands. 6. Department of Ophthalmology, VU University Medical Center, Amsterdam, the Netherlands. 7. Department of Epidemiology and Biostatistics, EMGO+ Institute, VU University Medical Center, Amsterdam, the Netherlands.
Abstract
OBJECTIVE: Patients with longstanding type 1 diabetes may develop microangiopathy due to high cumulative glucose exposure. Also, chronic hyperglycemia is related to cerebral alterations and cognitive dysfunction. Whether the presence of microangiopathy is conditional to the development of hyperglycemia-related cerebral compromise is unclear. Since subcortical, rather than cortical, volume loss was previously related to cognitive dysfunction in other populations, we measured these brain correlates and cognitive functions in patients with longstanding type 1 diabetes with and without microangiopathy. RESEARCH DESIGN AND METHODS: We evaluated differences in subcortical volume and cortical thickness and volume in type 1 diabetic patients with (n = 51) and without (n = 53) proliferative retinopathy and 49 control subjects and related volume differences to cognitive dysfunction. Analyses were corrected for age, sex, systolic blood pressure, and A1C. RESULTS: Putamen and right thalamic volume loss was noted in both patients with and without proliferative retinopathy compared with control subjects (all P < 0.05). Additionally, in patients with proliferative retinopathy relative to control subjects, volume loss of the bilateral nucleus accumbens was found (all P < 0.05). No differences were observed between the two patient groups. Cortical thickness and volume were not different between groups. In pooled analyses, lower left nucleus accumbens volume was associated with cognitive dysfunction (P < 0.035). CONCLUSIONS: This study shows subcortical, but not cortical, volume loss in relation to cognitive dysfunction in patients with longstanding type 1 diabetes, irrespective of microangiopathy. The time course, pathophysiology, and clinical relevance of these findings need to be established in longitudinal and mechanistic studies.
OBJECTIVE:Patients with longstanding type 1 diabetes may develop microangiopathy due to high cumulative glucose exposure. Also, chronic hyperglycemia is related to cerebral alterations and cognitive dysfunction. Whether the presence of microangiopathy is conditional to the development of hyperglycemia-related cerebral compromise is unclear. Since subcortical, rather than cortical, volume loss was previously related to cognitive dysfunction in other populations, we measured these brain correlates and cognitive functions in patients with longstanding type 1 diabetes with and without microangiopathy. RESEARCH DESIGN AND METHODS: We evaluated differences in subcortical volume and cortical thickness and volume in type 1 diabeticpatients with (n = 51) and without (n = 53) proliferative retinopathy and 49 control subjects and related volume differences to cognitive dysfunction. Analyses were corrected for age, sex, systolic blood pressure, and A1C. RESULTS: Putamen and right thalamic volume loss was noted in both patients with and without proliferative retinopathy compared with control subjects (all P < 0.05). Additionally, in patients with proliferative retinopathy relative to control subjects, volume loss of the bilateral nucleus accumbens was found (all P < 0.05). No differences were observed between the two patient groups. Cortical thickness and volume were not different between groups. In pooled analyses, lower left nucleus accumbens volume was associated with cognitive dysfunction (P < 0.035). CONCLUSIONS: This study shows subcortical, but not cortical, volume loss in relation to cognitive dysfunction in patients with longstanding type 1 diabetes, irrespective of microangiopathy. The time course, pathophysiology, and clinical relevance of these findings need to be established in longitudinal and mechanistic studies.
Authors: Eelco van Duinkerken; Menno M Schoonheim; Richard G IJzerman; Annette C Moll; Jesus Landeira-Fernandez; Martin Klein; Michaela Diamant; Frank J Snoek; Frederik Barkhof; Alle-Meije Wink Journal: Hum Brain Mapp Date: 2017-04-21 Impact factor: 5.038
Authors: Eelco van Duinkerken; Richard G Ijzerman; Martin Klein; Annette C Moll; Frank J Snoek; Philip Scheltens; Petra J W Pouwels; Frederik Barkhof; Michaela Diamant; Betty M Tijms Journal: Hum Brain Mapp Date: 2015-12-23 Impact factor: 5.038
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Authors: C Moran; R J Tapp; A D Hughes; C G Magnussen; L Blizzard; T G Phan; R Beare; N Witt; A Venn; G Münch; B C Amaratunge; V Srikanth Journal: J Diabetes Res Date: 2016-05-25 Impact factor: 4.011
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