Type 2 diabetes (T2D) is now recognized as an independent risk factor for accelerated cognitive decline and neurological conditions like Alzheimer’s disease. Less is known about the neurocognitive function of T2D patients with comorbid metabolic syndrome, despite their elevated risk for impairment. Computerized testing in 47 adults with T2D that met criteria for NCEP metabolic syndrome revealed that cognitive impairment was prevalent, including 13% in tests of memory, 50% in attention, and 35% in executive function. Partial correlations showed that longer duration of diabetes was associated with poorer performance on tests of basic attention ( ), working memory ( ), and executive function ( ). Strong associations between very low density lipoprotein and poor cognitive function also emerged, including tests of set shifting ( ) and cognitive inhibition ( ). Findings suggest that patients with T2D that meet criteria for metabolic syndrome are at high risk for cognitive impairment. Prospective studies should look to replicate these findings and examine the possible neuroprotective effects of lipid-lowering medication in this population. 1. Introduction Type 2 diabetes (T2D) is a metabolic disorder characterized by peripheral insulin resistance and reduced insulin production. The resulting hyperglycemia can lead to both microvascular complications, such as neuropathy, nephropathy, and retinopathy, and macrovascular complications, such as cardiovascular disease and stroke [1]. In addition to these complications, a growing number of studies demonstrate that T2D also has adverse effects on the brain, including elevated risk for conditions such as stroke and dementia [2–7]. More recent work shows that cognitive impairment is found in people with T2D long prior to the onset of these conditions, with impairments on tasks of memory and executive function being likely [8–10]. A better understanding of these cognitive impairments has important clinical implications, as they have recently been linked to poorer disease self-management [11]. The mechanisms contributing to cognitive changes in T2D remain poorly understood. Several parameters, particularly hyperglycemia [12, 13], have been proposed as potential risk factors for cognitive decline in type 2 diabetics. In the Memory in Diabetes (MIND) substudy of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, for example, Launer et al. [14] found an association between glycated hemoglobin (HbA1c), a marker of chronic hyperglycemia, and lower cognitive function in patients with T2D. Despite this
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