OBJECTIVE: Aim of the study was to compare plasma glucose concentrations and insulin resistance indices among patients with Alzheimer's disease (AD), frontotemporal lobar degeneration (FTLD) and controls. BACKGROUND: Growing evidence suggests that insulin and glucose metabolism may contribute to cognitive impairment and neurodegeneration. Biological mechanisms underlying this association are still scantly known. Recent studies demonstrated that an impairment of central insulin signaling plays a key role in AD pathogenesis. Insulin sensitivity has not yet been investigated in patients with FTLD. DESIGN/METHODS: 21 AD patients (9 men, 12 women, mean age ± SD = 68.2 ± 9.5 yrs) and 16 FTLD patients (9 men, 7 women, mean age ± SD = 63.8 ± 7.3 yrs) were selected for the study and compared with a group of 21 controls. All patients underwent CSF measurement of T-tau, p-Tau and A??1-42. A 75 g oral glucose tolerance test (OGTT) was performed. Indices of beta cell function and insulin sensitivity (HOMA-IR, QUICKI, ISI-composite, ISI-Stumvoll and OGIS-180) were calculated. RESULTS: During OGTT, glucose were significantly higher both in AD and FTLD than in controls. Plasmatic insulin levels were significantly reduced in AD patients compared with controls only at baseline and at 30', while in FTLD insulin concentrations were slightly increased. ISI-composite, HOMA-IR and OGIS-180 were significantly altered in AD patients compared to controls. ISI-Stumvoll and OGIS-180 indices were different in FTLD patients in comparison with controls. CONCLUSIONS: We found that glucose concentrations during the OGTT test and indices of insulin sensitivity were significantly impaired both in AD and FTLD patients. Intriguingly, plasmatic insulin concentration showed two different patterns in AD and FTLD, with an early impaired insulin secretion in AD and a delayed hyperinsulinemic response to glucose administration in FTLD. Our preliminary data supports the hypothesis that, in addition to AD, insulin resistance plays a role also in FTLD pathogenesis.
Insulin Resistance in Dementia: A Comparison between Alzheimer's Disease and Frontotemporal Lobar Degeneration
RAINERO, Innocenzo;RUBINO, Elisa;NEGRO, ELISA;VACCA, Alessandro;GOVONE, Flora;PINESSI, Lorenzo
2012-01-01
Abstract
OBJECTIVE: Aim of the study was to compare plasma glucose concentrations and insulin resistance indices among patients with Alzheimer's disease (AD), frontotemporal lobar degeneration (FTLD) and controls. BACKGROUND: Growing evidence suggests that insulin and glucose metabolism may contribute to cognitive impairment and neurodegeneration. Biological mechanisms underlying this association are still scantly known. Recent studies demonstrated that an impairment of central insulin signaling plays a key role in AD pathogenesis. Insulin sensitivity has not yet been investigated in patients with FTLD. DESIGN/METHODS: 21 AD patients (9 men, 12 women, mean age ± SD = 68.2 ± 9.5 yrs) and 16 FTLD patients (9 men, 7 women, mean age ± SD = 63.8 ± 7.3 yrs) were selected for the study and compared with a group of 21 controls. All patients underwent CSF measurement of T-tau, p-Tau and A??1-42. A 75 g oral glucose tolerance test (OGTT) was performed. Indices of beta cell function and insulin sensitivity (HOMA-IR, QUICKI, ISI-composite, ISI-Stumvoll and OGIS-180) were calculated. RESULTS: During OGTT, glucose were significantly higher both in AD and FTLD than in controls. Plasmatic insulin levels were significantly reduced in AD patients compared with controls only at baseline and at 30', while in FTLD insulin concentrations were slightly increased. ISI-composite, HOMA-IR and OGIS-180 were significantly altered in AD patients compared to controls. ISI-Stumvoll and OGIS-180 indices were different in FTLD patients in comparison with controls. CONCLUSIONS: We found that glucose concentrations during the OGTT test and indices of insulin sensitivity were significantly impaired both in AD and FTLD patients. Intriguingly, plasmatic insulin concentration showed two different patterns in AD and FTLD, with an early impaired insulin secretion in AD and a delayed hyperinsulinemic response to glucose administration in FTLD. Our preliminary data supports the hypothesis that, in addition to AD, insulin resistance plays a role also in FTLD pathogenesis.
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