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PMID |
Sentence |
1 |
15850385
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Deletion of insulin-degrading enzyme (IDE) in mice causes accumulation of cerebral amyloid beta-protein (Abeta), hyperinsulinemia, and glucose intolerance.
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2 |
16399206
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We review the current evidence, which suggests that hyperinsulinaemia may elevate Abeta through insulin's competition with Abeta for IDE.
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3 |
17609417
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The apparent hepatic uptake of [(125)I]Abeta(1-40) was also induced by insulin in a time-dependent manner.
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4 |
17609417
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In conclusion, plasma insulin facilitates LRP-1 translocation to the hepatic plasma membrane from the intracellular pool, resulting in significant enhancement of hepatic Abeta(1-40) uptake from the circulating blood.
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5 |
19387119
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Insulin influences Abeta production by modulating alpha-secretase activity and Abeta degradation.
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6 |
19672057
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We recently demonstrated that adipocyte amyloid precursor protein (APP) expression is upregulated in obesity and correlates with insulin resistance and adipose tissue inflammation.
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7 |
19672057
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At baseline, adipocyte APP expression correlated significantly with plasma Abeta40 levels and with 2-hour insulin concentrations.
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8 |
19672057
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Changes in adipocyte APP expression correlated with changes in plasma Abeta40 levels (R = 0.74, p = 0.01) and changes in 2-hour insulin (R = 0.75, p = 0.01).
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9 |
19936237
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There is increasing evidence that insulin also plays a role in Alzheimer's disease (AD) as it is involved in the metabolism of beta-amyloid (Abeta) and tau, two proteins that form Abeta plaques and neurofibrillary tangles (NFTs), respectively, the hallmark lesions in AD.
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10 |
19237574
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In addition, we found that glucose deprivation and various tyrphostins, known inhibitors of insulin-like growth factors/insulin receptor tyrosine kinases, do not modulate the effect of metformin on Abeta.
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11 |
16444902
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Insulin and IGF-I may modulate brain levels of insulin degrading enzyme, which would also lead to an accumulation of Abeta amyloid.
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12 |
21411544
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Insulin infusion significantly suppressed the expression of APP, presenilin-1, presenilin-2, and glycogen synthase kinase-3? in peripheral blood mononuclear cells.
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