RESUMEN
Background/Aims. Diabetes might increase the risk of Alzheimer's disease (AD). For detecting dementia, it is typical to obtain informants' perceptions of cognitive deficits, but such interviews are usually difficult in routine care. We aimed to develop a model for predicting mild to moderate AD using a self-reported questionnaire and by evaluating vascular risk factors for dementia in elderly subjects with diabetes. Methods. We recruited 286 diabetic and 155 nondiabetic elderly subjects. There were 25 patients with AD and 261 cognitively normal individuals versus 30 with AD and 125 normal subjects, respectively. Each participant answered subjective questions on memory deficits and daily functioning. Information on vascular risk factors was obtained from clinical charts, and multivariate logistic regression was used to develop a model for predicting AD. Results. The predicted probabilities used in screening for AD in diabetic subjects constituted age, education, lower diastolic blood pressure, subjective complaints of memory dysfunction noticeable by others, and impaired medication, shopping, and travel outside a familiar locality. Receiver operating characteristic analysis revealed a satisfactory discrimination for AD specific for diabetic elderly subjects, with 95.2% sensitivity and 90.6% specificity. Conclusion. This is the first useful index that can prescreen for AD in elderly subjects with diabetes.
Asunto(s)
Neuropatías Diabéticas/etiología , Nervios Periféricos/irrigación sanguínea , Aldehído Reductasa/antagonistas & inhibidores , Animales , Capilares/fisiopatología , Permeabilidad Capilar , Neuropatías Diabéticas/terapia , Inhibidores Enzimáticos/uso terapéutico , Terapia Genética , Factor de Crecimiento de Hepatocito/genética , Humanos , Isquemia , Estrés Oxidativo , Flujo Sanguíneo Regional , Daño por Reperfusión/etiología , Rodanina/análogos & derivados , Rodanina/uso terapéutico , Tiazolidinas , Factor A de Crecimiento Endotelial Vascular/genéticaRESUMEN
A fetus in the uterus is not rejected at any time during the entire gestational period, even without the administration of immunosuppressive agents, though fetus is a kind of allograft. This prevention of rejection is considered to be associated with the presence of placental tissues. This hypothesis was tested by the allografting of islets together with placental tissues (trophoblasts) in streptozotocin (STZ)-induced diabetic mice. Placentae were harvested from the mice at the 14th postgestation day by being peeled off carefully and with the maternal decidua left behind, and cut into small pieces. Five hundred freshly isolated islets together with placental tissues obtained from ICR mice were placed under the left kidney capsule of STZ-induced diabetic C57BL/6J mice. The nonfasting blood glucose level was reduced from 477 +/- 41 mg/dl at the time of pretransplant to that of the intact normal mice (161 +/- 18 mg/dl) soon after the cografting, and did not return to the pretransplant level before the 14th posttransplant day. The grafting of the same number of islets alone and/or liver tissues dropped the blood glucose level, but not to that of the intact normal mice. It returned to the pretransplant level within 1 week. This is the first successful prolongation of survival of allografted islets without immunosuppressive agents through cotransplantation of allogenic placental tissues. The underlying mechanism remains to be clarified.