| 1. |
- Evered, Lisbeth, et al.
(författare)
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Cerebrospinal Fluid Biomarker for Alzheimer Disease Predicts Postoperative Cognitive Dysfunction.
- 2016
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Ingår i: Anesthesiology. - 1528-1175. ; 124:2
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Tidskriftsartikel (refereegranskat)abstract
- Postoperative cognitive dysfunction (POCD) affects 16 to 21% of the elderly 3 months after anesthesia and surgery and is associated with adverse outcomes. The exact cause of POCD remains unknown. The authors hypothesized that elderly individuals with Alzheimer disease (AD) neuropathology, identified by cerebrospinal fluid (CSF) analysis, would have increased the risk for POCD.
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| 2. |
- Insel, Philip S., et al.
(författare)
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Determining clinically meaningful decline in preclinical Alzheimer disease
- 2019
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Ingår i: Neurology. - 1526-632X. ; 93:4, s. 322-333
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To determine the time required for a preclinical Alzheimer disease population to decline in a meaningful way, use estimates of decline to update previous clinical trial design assumptions, and identify factors that modify β-amyloid (Aβ)-related decline. METHODS: In 1,120 cognitively unimpaired individuals from 3 international cohorts, we estimated the relationship between Aβ status and longitudinal changes across multiple cognitive domains and assessed interactions between Aβ and baseline factors. Power analyses were performed to explore sample size as a function of treatment effect. RESULTS: Cognitively unimpaired Aβ+ participants approach mild cognitive impairment (MCI) levels of performance 6 years after baseline, on average. Achieving 80% power in a simulated 4-year treatment trial, assuming a 25% treatment effect, required 2,000 participants/group. Multiple factors interacted with Aβ to predict cognitive decline; however, these findings were all cohort-specific. Despite design differences across the cohorts, with large sample sizes and sufficient follow-up time, the Aβ+ groups declined consistently on cognitive composite measures. CONCLUSIONS: A preclinical AD population declines to the cognitive performance of an early MCI population in 6 years. Slowing this rate of decline by 40%-50% delays clinically relevant impairment by 3 years-a potentially meaningful treatment effect. However, assuming a 40%-50% drug effect highlights the difficulties in preclinical AD trial design, as a more commonly assumed treatment effect of 25% results in a required sample size of 2,000/group. Designers of preclinical AD treatment trials need to prepare for larger and longer trials than are currently being considered. Interactions with Aβ status were inconsistent and not readily generalizable.
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| 3. |
- McGuckian, Thomas B., et al.
(författare)
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Development of complex executive function over childhood : Longitudinal growth curve modeling of performance on the Groton Maze Learning Task
- 2023
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Ingår i: Child Development. - : John Wiley & Sons. - 0009-3920 .- 1467-8624. ; 94:3, s. 648-658
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Tidskriftsartikel (refereegranskat)abstract
- This longitudinal study modeled children's complex executive function (EF) development using the Groton Maze Learning Task (GMLT). Using a cohort-sequential design, 147 children (61 males, 5.5–11 years) were recruited from six multicultural primary schools in Melbourne and Perth, Australia. Race/ethnicity data were not available. Children were assessed on the GMLT at 6-month intervals over 2-years between 2010 and 2012. Growth curve models describe age-related change from 5.5 to 12.5 years old. Results showed a quadratic growth trajectory on each measure of error—that is, those that reflect visuospatial memory, executive control (or the ability to apply rules for action), and complex EF. The ability to apply rules for action, while a rate-limiting factor in complex EF, develops rapidly over early-to-mid childhood.
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| 4. |
- Sathiavageeswaran, Mahesh, et al.
(författare)
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Effects of GH on cognitive function in elderly patients with adult-onset GH deficiency: a placebo-controlled 12-month study
- 2007
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Ingår i: European Journal of Endocrinology. - : Oxford University Press (OUP). - 1479-683X .- 0804-4643. ; 156:4, s. 439-447
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Young adults with childhood-onset GH deficiency (GHD) have reduced memory and attention, which can be improved by treatment with GH. Little information is available on cognitive function in elderly GHD patients. Design: Single center, double-blind, randomized, placebo-controlled study of 52-week duration. Methods: Elderly GH therapy naive GHD patients (n = 34; age range 60-77 years) were enrolled and randomized to receive placebo or GH therapy which was titrated to achieve a target IGF-I level of + 1 to + 2 S.D. of the normal mean for age. Cognitive function was assessed at baseline and after 24 and 52 weeks, using a computerized psychometric test package (Neurobehavioral Examination System-2). Results: The mean GH dose was 0.16 +/- 0.06 mg/day; mean IGF-I increased from 135 +/- 59 ng/ml at baseline to 213 + 77 ng/ml during active treatment. The GH-treated group had better mean serial digit learning scores compared with placebo group (P < 0.05). Assessment of effect sizes showed that improvements in memory occurred with GH after 24 weeks. The overall adverse event rates were similar in the GH and the placebo group. Conclusion: This study indicates that GH replacement may be accompanied by improvement in certain measures of cognitive function in elderly patients with GHD.
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