IGFI and Insulin Receptor Levels in Cognition

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No significant differences are found in IGF-I or insulin receptor levels in any subfields of the hippocampus of young versus aged rats (Doré, Kar, Rowe, & Quirion, 1997). Furthermore, deficits in cognitive performance do not relate to alterations in the levels of these receptors in aged impaired (AI) compared to aged unimpaired (AU) rats. It thus appears that IGF-I and insulin receptor binding sites are not markedly altered during the normal aging process in rats, and cognitive deficits observed in the Morris water maze are not mirrored by changes in these markers. Accordingly, spatial learning deficits observed in the AI group are not due to alteration in IGFs and/or insulin receptor sites. However, these data do not rule out the potential of altered IGFs or insulin postreceptor signaling efficacy between AU and AI groups (discussed later). These results can also be related to those obtained in the human brain. No significant differences in the levels of IGF-I binding sites were reported in the human cerebral cortex with respect to age, postmortem delays, or medications (Crews, McElhaney, Freund, Ballinger, & Raizada, 1992). In contrast, specific IGF-I binding was increased in the cerebral cortex of Alzheimer's disease (AD) patients, possibly in response to decreased levels of IGF-I (Jafferali, Dumont, Sotty, Robitaille, Quirion, & Kar, 2000).

Regarding insulin receptors, an earlier study reported results similar in 22-month-old (compared to young) Wis-tar rats, with no significant changes being observed in any brain regions, except for a slight decrement in olfactory bulbs (Tchilian, Zhelezarov, Petkov, & Hadjiivanova, 1990). In contrast, insulin receptor binding was reported to be decreased in aged mouse brain homogenates (Zaia & Pi-antanelli, 1996). These differences are likely to be species-related. A study on the ontogenesis of the insulin receptor using synaptosomal membranes revealed a general decrease in the human cerebral cortex from development to adulthood (Potau, Escofet, & Martinez, 1991).

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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