Enhancement of Memory in Alzheimer Disease With Insulin and Somatostatin, but Not Glucose

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Abstract
ALZHEIMER disease (AD) is accompanied by disrupted glucose metabolism and insulin resistance that may contribute to its characteristic memory impairment.1-3 Increasing glucose availability by raising plasma glucose levels improves memory for new information in patients with AD.2,4-6 Such memory facilitation is associated with a glucose-stimulated elevation in endogenous insulin levels, raising the question of whether improvement is due to changes in insulin, independent of hyperglycemia. In previous work, we have demonstrated that raising insulin levels while keeping plasma glucose at fasting baseline levels was sufficient to improve memory for patients with AD.2 However, the question remains whether raising plasma glucose levels alone without an accompanying elevation in insulin is also sufficient to enhance memory. This question is of considerable theoretical import. Although numerous studies have demonstrated that raising plasma glucose to an optimal level improves memory for healthy adults and patients with AD,7 insulin effects on cognitive abilities such as memory have only been recently demonstrated.2 Indeed, the question of whether and how the brain is affected by insulin is controversial. A potential role for insulin in the brain is supported by documentation of dense insulin receptor distributions in several brain regions, including the CA1, CA3, and dentate gyrus regions of the hippocampus, entorhinal cortex, hypothalamus, and olfactory bulb.8,9 Interestingly, these regions are also affected earliest and most severely in patients with AD.

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