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Версія від 07:32, 18 березня 2017, створена Yarn43angle (обговореннявнесок) (Створена сторінка: For the 11 participants at risk of familial AD, the etiology was determined by considering whether or not a familial AD mutation was present in combination with...)

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For the 11 participants at risk of familial AD, the etiology was determined by considering whether or not a familial AD mutation was present in combination with clinical factors (e.g., their age relative to the typical age of AD symptom onset in their family and the presence of other conditions which might account for their performance). PI3K inhibitor Statistical Analyses Analysis of variance (ANOVA) was used to test for differences in demographics and MoCA scores among diagnostic groups. For the nominal variable gender, the ��2 test was used. After examining the pattern of diagnosis-adjusted MoCA residuals in relation to education, we applied four alternative education-based adjustments for the raw score of the MoCA. To compare the effect of different adjustments, we used bootstrap sampling and examined two criteria: (1) the SD of the residuals, and (2) the association between education and the residuals. Sensitivity and specificity analyses were also carried out for the raw and each adjusted score using several cutoffs. Finally, we evaluated the psychometric properties of the MoCA. We computed Cronbach's �� coefficient and item-total correlations to examine the internal reliability and item discrimination power, respectively. To examine item validity, we used the clinical diagnosis as an external standard and performed ANOVA to test for item score differences among diagnostic groups. The effects of education on item scores was tested with a regression model for each item score adjusting Selleck Staurosporine for diagnosis. We performed two-tailed Student's t test to identify items most sensitive to cognitive impairment due to probable or possible AD, relative to the normal controls. Sensitivity and specificity analyses were performed in R using library ��ROCR�� [21]. All the other analyses were performed in SAS. Results Six participants were diagnosed as cognitively normal, 18 as MCI, 3 as ��impaired but not MCI��, and 23 as dementia. The presumed etiologies for the cognitively impaired and the demented participants can been seen in table ?table11. Table 1 Diagnosis and presumed etiology in the study sample The MCI and ��impaired but not MCI�� groups were combined to create the cognitively impaired not demented (CIND) group. Demographics and MoCA raw scores for the three diagnostic groups are shown in table ?table2.2. The groups did not differ in gender composition Resminostat (��2 = 1.44, p = 0.49) or years of education (F = 1.10, p = 0.34). There was an age difference (F = 9.69, p