Glucose And Memory

The beneficial effects of glucose administration on memory have been well documented, as reviewed by Messier (4). Nearly three decades ago, Lapp demonstrated in teenagers that acute glucose administration could facilitate memory (5). Since then, researchers have shown in animals and humans that the beneficial effects of elevating plasma glucose levels on learning and memory are dependent on an optimal dose, the type of sugar, task demands, gender, age, cognitive status, and the relative timing of glucose administration and task (3, 4). These glucose effects are consistent with observations that the brain supply of glucose is derived from peripheral circulation and that glucose is the brain's principal energy substrate (6). Glucose-induced memory facilitation has been observed in both healthy older adult humans and persons with Alzheimer's disease (3, 7). For example, Craft et al. gave patients with Alzheimer's disease an oral glucose load of 75 g and showed improved memory for patients with a specific glucoreg-ulatory profile.

In contrast to acute hyperglycemia, chronic hyperglycemia exerts detrimental effects on cognition. T2DM and its precursor, impaired glucose tolerance, are common among aging adults. Adults above age 60 run a one in five chance of having T2DM (8) and a one in three chance of having either impaired glucose tolerance or T2DM (9). Most, though not all, studies have detected cognitive changes associated with T2DM (10-13). In older adults with T2DM, the most common cognitive deficit is a decline in list learning (12); other areas affected by diabetes may include attention, manual dexterity, reasoning, and psychomotor speed (10-13). Furthermore, there is evidence from rodents and humans that abnormal glucoregulation in the absence of diabetes can impair memory and global cognitive functioning (14-16). It is important to note that cognitive deficits associated with diabetes may, in part, be reversible with treatment for diabetes (11,17-19).

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