![]() ![]() Of the 30 T2DM patients, 6 were under treatment with insulin and 24 controlled blood glucose with oral hypoglycemic agents (17 with glucosidase inhibitors, 4 with gliquidone, 3 with biguanides). FPG, glycosylated hemoglobin (HbA 1c), and cholesterol levels were measured by standard laboratory testing. All participants underwent a medical history and physical examination during which height, weight, and body mass index (BMI) were recorded. T2DM was diagnosed using established criteria on the basis of patients’ medical histories, medication use, or fasting plasma glucose (FPG) levels (≥7 mmol/L) ( 18). ![]() Sixty-seven participants met these criteria, including 30 patients with diabetes and 37 healthy control participants. In this cross-sectional study, all participants were selected according to the following criteria: 1) no less than 6 years of education 2) scores ≥24 on the mini-mental state examination (MMSE), Chinese version 3) no history of coronary disease, nephritis, tumors, gastrointestinal disease, or psychiatric illness and 4) ability to meet the physical demands of the imaging procedure. The participants in this study were all from the Beijing Aging Brain Rejuvenation Initiative (BABRI), which is an ongoing, longitudinal study investigating aging and cognitive impairment in urban elderly people in Beijing, China. Thus, it is conceivable that cognitive functions such as WM are particularly susceptible to the effects of aging and some diseases, including AD ( 12). However, AD and MCI patients may exhibit more activation than control subjects in the right frontal and bilateral middle frontal gyri in another visual WM task, suggesting compensation for decreased neural efficiency ( 11). A previous functional magnetic resonance imaging (fMRI) study demonstrated that during an n-back task assessing WM, patients with MCI exhibited reduced activation in the frontoparietal regions compared with control subjects ( 10). In older adults, the behavioral testing of WM has been associated with extent of frontal activation, which may suggest that the decreased frontal cortex contributions to cognitive experience ultimately result in age-associated decreases in memory ability ( 9). There has been growing interest in detecting how WM is influenced during aging and in AD and mild cognitive impairment (MCI). Some studies have shown that WM deficits furtively emerge with the early pathology that involves the accumulation of neuritic plaques and neurofibrillary tangles in the frontal cortex ( 8). As proposed by Baddeley ( 7), WM provides the temporary storage of and operations on information necessary for advanced cognition. Given that AD is a high-incidence disease of elderly people, WM impairment is generally a considerable cognitive deficit of AD throughout the development of the disease. Many cognitive performances, such as working memory (WM), deteriorate in older adults compared with younger adults and teenagers ( 6). ![]()
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