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Ventral striatum, but not cortical volume loss, is related to cognitive dysfunction in type 1 diabetic patients with
Eelco van Duinkerken1, Menno M Schoonheim2, Martijn D Steenwijk3
1Diabetes 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.
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.
Insights
Longstanding type 1 diabetes is linked to subcortical brain volume loss and cognitive dysfunction, regardless of microangiopathy. This study highlights changes in the putamen, thalamus, and nucleus accumbens, impacting cognitive function in diabetic patients.
Area of Science:
- Neuroscience
- Endocrinology
- Diabetology
Background:
- Longstanding type 1 diabetes can lead to microangiopathy and cognitive dysfunction due to chronic hyperglycemia.
- The relationship between microangiopathy and hyperglycemia-induced brain changes remains unclear.
- Subcortical volume loss, not cortical, is associated with cognitive impairment in other populations.
Purpose of the Study:
- To investigate subcortical and cortical brain volume differences in type 1 diabetes patients with and without microangiopathy.
- To determine the association between these brain changes and cognitive function.
Main Methods:
- Compared subcortical volume, cortical thickness, and volume in type 1 diabetes patients (with/without proliferative retinopathy) and controls.
- Performed analyses adjusted for age, sex, blood pressure, and A1C.
- Correlated brain volume differences with cognitive dysfunction.
Main Results:
- Both type 1 diabetes groups showed putamen and right thalamic volume loss compared to controls.
- Patients with proliferative retinopathy also exhibited bilateral nucleus accumbens volume loss.
- No significant differences in cortical thickness or volume were observed between groups.
- Lower left nucleus accumbens volume correlated with cognitive dysfunction in pooled analyses.
Conclusions:
- Subcortical, not cortical, brain volume loss is associated with cognitive dysfunction in longstanding type 1 diabetes.
- These brain changes occur irrespective of microangiopathy status.
- Further longitudinal and mechanistic studies are needed to understand the clinical relevance and pathophysiology.
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