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Sökning: WFRF:(Maruff Paul)

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1.
  • Evered, Lisbeth, et al. (författare)
  • Cerebrospinal Fluid Biomarker for Alzheimer Disease Predicts Postoperative Cognitive Dysfunction.
  • 2016
  • Ingår i: Anesthesiology. - 1528-1175. ; 124:2
  • 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)
  • Determining clinically meaningful decline in preclinical Alzheimer disease
  • 2019
  • Ingår i: Neurology. - American Academy of Neurology. - 1526-632X. ; 93:4, s. 322-333
  • 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.
3.
  • Knopman, David S., et al. (författare)
  • The National Institute on Aging and the Alzheimer's Association Research Framework for Alzheimer's disease : Perspectives from the Research Roundtable
  • 2018
  • Ingår i: Alzheimer's and Dementia. - Wiley. - 1552-5260. ; 14:4, s. 563-575
  • Forskningsöversikt (refereegranskat)abstract
    • The Alzheimer's Association's Research Roundtable met in November 2017 to explore the new National Institute on Aging and the Alzheimer's Association Research Framework for Alzheimer's disease. The meeting allowed experts in the field from academia, industry, and government to provide perspectives on the new National Institute on Aging and the Alzheimer's Association Research Framework. This review will summarize the “A, T, N System” (Amyloid, Tau, and Neurodegeneration) using biomarkers and how this may be applied to clinical research and drug development. In addition, challenges and barriers to the potential adoption of this new framework will be discussed. Finally, future directions for research will be proposed.
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4.
  • Sathiavageeswaran, Mahesh, et al. (författare)
  • Effects of GH on cognitive function in elderly patients with adult-onset GH deficiency: a placebo-controlled 12-month study
  • 2007
  • Ingår i: European Journal of Endocrinology. - Society of the European Journal of Endocrinology. - 1479-683X. ; 156:4, s. 439-447
  • 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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5.
  • Vermunt, Lisa, et al. (författare)
  • Duration of preclinical, prodromal, and dementia stages of Alzheimer's disease in relation to age, sex, and APOE genotype
  • 2019
  • Ingår i: Alzheimer's & Dementia. - Elsevier. - 1552-5260 .- 1552-5279. ; 15:7, s. 888-898
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>INTRODUCTION:</strong> We estimated the age-specific duration of the preclinical, prodromal, and dementia stages of Alzheimer's disease (AD) and the influence of sex, setting, apolipoprotein E (APOE) genotype, and cerebrospinal fluid tau on disease duration.</p><p><strong>METHODS:</strong> We performed multistate modeling in a combined sample of 6 cohorts (n = 3268) with death as the end stage and estimated the preclinical, prodromal, and dementia stage duration.</p><p><strong>RESULTS:</strong> The overall AD duration varied between 24 years (age 60) and 15 years (age 80). For individuals presenting with preclinical AD, age 70, the estimated preclinical AD duration was 10 years, prodromal AD 4 years, and dementia 6 years. Male sex, clinical setting, APOE ε4 allele carriership, and abnormal cerebrospinal fluid tau were associated with a shorter duration, and these effects depended on disease stage.</p><p><strong>DISCUSSION:</strong> Estimates of AD disease duration become more accurate if age, sex, setting, APOE, and cerebrospinal fluid tau are taken into account. This will be relevant for clinical practice and trial design.</p>
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