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
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