Cognitive functioning depends on intact brain networks that can be assessed with functional magnetic resonance imaging (fMRI) techniques. We hypothesized that cognitive decrements in type 1 diabetes mellitus (T1DM) are associated with alterations in resting-state neural connectivity and that these changes vary according to the degree of microangiopathy. T1DM patients with (MA+: n = 49) and without (MA−: n = 52) microangiopathy were compared with 48 healthy control subjects. All completed a neuropsychological assessment and resting-state fMRI. Networks were identified using multisubject independent component analysis; specific group differences within each network were analyzed using the dual-regression method, corrected for confounding factors and multiple comparisons. Relative to control subjects, MA− patients showed increased connectivity in networks involved in motor and visual processes, whereas MA+ patients showed decreased connectivity in networks involving attention, working memory, auditory and language processing, and motor and visual processes. Better information-processing speed and general cognitive ability were related to increased degree of connectivity. T1DM is associated with a functional reorganization of neural networks that varies, dependent on the presence or absence of microangiopathy.

Mild cognitive dysfunction is a well-established complication of diabetes and its management, although large numbers of psychologists and health professionals may be unaware of its existence, clinical implications, and etiology. Drawing on results from key studies, systematic reviews, and meta-analyses, this article delineates the neurocognitive phenotypes characteristic of Type 1 diabetes (T1D) and Type 2 diabetes (T2D), and identifies the most plausible risk factors, both those that may be modifiable, like degree of metabolic control, and those that cannot be changed, like the age when a child or adult is diagnosed. Most children and adults with T1D typically manifest lower scores on measures of intelligence and academic achievement, attention, psychomotor speed, and executive functions. These effects are especially pronounced in those who develop diabetes early in life, before the age of 6 or 7 years. Chronically elevated blood glucose values increase the risk of both cognitive dysfunction and microstructural changes in white matter tracts. Adults with T2D manifest cognitive dysfunction characterized by poorer performance on tasks requiring attention, psychomotor speed, planning and executive functions, and learning and memory. They are also at increased risk of developing dementia. Poorer metabolic control accelerates the rate of cognitive decline over time, and research suggests that improving metabolic control may slow the rate of decline. Psychologists and behavioral scientists can play a key role in preventing the onset of cognitive complications or in ameliorating their severity by implementing behavioral strategies known to increase adherence to medical regimens and improve metabolic control. (PsycINFO Database Record

Type 2 diabetes mellitus (T2DM) is characterized by obesity, hyperglycemia and insulin resistance. Both T2DM and obesity are associated with cerebral complications, including an increased risk of cognitive impairment and dementia, however the underlying mechanisms are largely unknown. In the current study, we aimed to determine the relative contributions of obesity and the presence of T2DM to altered white matter structure. We used diffusion tensor imaging (DTI) and voxel-based morphometry (VBM) to measure white matter integrity and volume in obese T2DM patients without micro- or macrovascular complications, age- gender- and BMI-matched normoglycemic obese subjects and age- and gender-matched normoglycemic lean subjects. We found that obese T2DM patients compared with lean subjects had lower axial diffusivity (in the right corticospinal tract, right inferior fronto-occipital tract, right superior longitudinal fasciculus and right forceps major) and reduced white matter volume (in the right inferior parietal lobe and the left external capsule region). In normoglycemic obese compared with lean subjects axial diffusivity as well as white matter volume tended to be reduced, whereas there were no significant differences between normoglycemic obese subjects and T2DM patients. Decreased white matter integrity and volume were univariately related to higher age, being male, higher BMI, HbA1C and fasting glucose and insulin levels. However, multivariate analyses demonstrated that only BMI was independently related to white matter integrity, and age, gender and BMI to white matter volume loss. Our data indicate that obese T2DM patients have reduced white matter integrity and volume, but that this is largely explained by BMI, rather than T2DM per se.

OBJECTIVEHyperglycemia-associated microvascular disease may underlie changes in cerebral functioning and cognitive performance in patients with type 1 diabetes. Functional connectivity, an indicator of functional interactions and information exchange between brain regions, provides a measure of cerebral functioning. This study addresses functional connectivity and cognition in type 1 diabetic patients with and without proliferative retinopathy, relative to healthy control subjects, using magnetoencephalography.RESEARCH DESIGN AND METHODSFluctuations in magnetic field at scalp for Δ, θ, lower and upper α, β, and lower and upper γ frequency bands were measured using magnetoencephalography. Synchronization likelihood, a measure of functional connectivity, was computed. Using neuropsychological tests, cognitive functioning was assessed and its associations with functional connectivity were determined.RESULTSCompared with control subjects, type 1 diabetic patients performed poorer on general cognitive ability, information processing speed, and motor speed, irrespective of their microvascular complication status. Functional connectivity, however, was lowest for type 1 diabetic patients with retinopathy, compared with type 1 diabetic patients without microvascular complications and control subjects, whereas type 1 diabetic patients without microvascular complications showed an increase relative to control subjects. Positive associations were found between functional connectivity and executive functioning, memory, information processing speed, motor speed, and attention.CONCLUSIONSCompared with healthy control subjects, functional connectivity and cognition differed in type 1 diabetic patients irrespective of microvascular complication status, indicating that chronic hyperglycemia, among other factors, may negatively affect brain functioning even before microvascular damage becomes manifest. The association found between synchronization likelihood and cognition suggests functional connectivity plays a significant role in cognitive functioning.

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OBJECTIVEWe investigated whether proliferative diabetic retinopathy in type 1 diabetic patients can be generalized to cerebral small vessel disease and whether it is associated with impaired peripheral microvascular function. RESEARCH DESIGN AND METHODSThirty-three patients with proliferative diabetic retinopathy (PDR+), 34 patients without proliferative diabetic retinopathy, and 33 controls underwent magnetic resonance imaging to assess cerebral microangiopathy (cerebral microbleeds) and ischemic damage (white matter hyperintensities and lacunes). Peripheral microvascular function, i.e., skin capillary density and capillary recruitment, was assessed by capillary microscopy. RESULTSCerebral microbleeds, but not ischemic damage, were more prevalent in PDR+ patients versus the other groups (P < 0.05). A trend was found across groups for the lowest baseline capillary density in PDR+ patients (P for trend = 0.05). In individuals with microbleeds, capillary recruitment was impaired compared with those without microbleeds (P = 0.04). CONCLUSIONSIn PDR+ patients, cerebral microbleed prevalence was higher and seems part of generalized microangiopathy that may affect the skin and the brain.

Decision-making is considered a fundamental aspect of personal autonomy and can be affected in psychiatric and neurologic diseases. It has been shown that cognitive deficits in dementia impact negatively on decision-making. Moreover, studies highlighted impaired clinical competence in neuropsychiatric disorders, such as schizophrenia and bipolar disorder. In this context, the current study explored the relationship between behavioral and psychological symptoms of dementia (BPSD) and clinical competence, especially the capacity to consent to treatment, in Alzheimer’s disease (AD). Seventy-one patients with mild to moderate AD participated, completing assessments for capacity to consent to treatment, general cognition and neuropsychiatric disturbances. For each neuropsychiatric symptom, patients with and without the particular disturbance were compared on the different subscales of the MacArthur Competence Tool for Treatment (MacCAT-T; Understanding, Appreciation, Reasoning and Expression). The results showed that patients presenting delusions, as well as apathetic patients, had a lower ability to express a clear treatment choice compared to patients without these symptoms. By contrast, patients with dysphoria/depression had higher scores on this variable. Additionally, AD patients with euphoria had more difficulties discussing consequences of treatment alternatives compared to patients without this disturbance. None of the differences were confounded by global cognition. There were no between-group differences in clinical decision-making for patients with hallucinations, agitation/aggression, anxiety, irritability, disinhibition and aberrant motor behavior. These findings highlight the importance of taking BPSD into account when assessing decision-making capacity, especially clinical competence, in AD. Furthermore, reducing BPSD may lead to better clinical competence in patients with AD, as well as to improvements in patients and caregivers’ quality of life.

OBJECTIVEPatients 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 METHODSWe 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. RESULTSPutamen 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). CONCLUSIONSThis 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.Longstanding type 1 diabetes mellitus may lead to development of microangiopathy, mediated by cumulative hyperglycemic exposure (1). Cognitive dysfunction is also related to prolonged hyperglycemia (2,3). Proliferative retinopathy, the presence of which has been found to be independently related to cognition and cerebral alterations