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Results Cohort 3.9% of group 1, 5% of group 2, and 8.4% of group 3 screened for the A4 trial. Significant differences were found among the groups (P  less then  0.001). Post hoc analyses showed differences in A4 screening rates between groups 1 and 3 (P  less then  0.001) and groups 2 and 3 (P = 0.0194). There were no differences in enrollment among the three groups. RCT 2.78% of the intervention group screened for A4 compared to 0% of controls (P = 0.0611). Discussion Online education via the AlzU.org digital tool may serve as an effective strategy to supplement clinical trial recruitment. © 2020 The Authors. Alzheimer's & Dementia Translational Research & Clinical Interventions published by Wiley Periodicals, Inc. on behalf of Alzheimer's Association.Therapeutic plasma exchange, consisting of removing blood plasma and exchanging it with donated blood products, has been proposed for treating Alzheimer's disease (AD) to remove senescent or toxic factors. In preclinical studies, administration of plasma from young healthy mice to AD transgenic mice improved cognitive deficits without affecting brain amyloid plaques. Initial encouraging results have been collected in a double-blind, placebo-controlled study in nine AD patients receiving young plasma. In a 14-month double-blind, placebo-controlled study in 322 AD patients, multiple infusions with plasma enriched with albumin with or without immunoglobulins slowed cognitive, functional, and clinical decline, especially in moderately affected patients. ABC294640 cell line Clinical trials of plasma fractions containing hypothetically beneficial proteins are also under way. These initial positive clinical results need to be confirmed in larger and more rigorous controlled studies in which the possible benefits of plasma exchange approaches can be weighed against the intrinsic side effects of repetitive infusion procedures. © 2020 The Authors. Alzheimer's & Dementia Translational Research & Clinical Interventions published by Wiley Periodicals, Inc. on behalf of Alzheimer's Association.Introduction The safety of predicting conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia using apolipoprotein E (APOE) genotyping is unknown. Methods We randomized 114 individuals with MCI to receive estimates of 3-year risk of conversion to AD dementia informed by APOE genotyping (disclosure arm) or not (non-disclosure arm) in a non-inferiority clinical trial. Primary outcomes were anxiety and depression scores. Secondary outcomes included other psychological measures. Results Upper confidence limits for randomization arm differences were 2.3 on the State Trait Anxiety Index and 0.5 on the Geriatric Depression Scale, below non-inferiority margins of 3.3 and 1.0. Moreover, mean scores were lower in the disclosure arm than non-disclosure arm for test-related positive impact (difference -1.9, indicating more positive feelings) and AD concern (difference -0.3). Discussion Providing genetic information to individuals with MCI about imminent risk for AD does not increase risks of anxiety or depression and may provide psychological benefits. © 2020 The Authors. Alzheimer's & Dementia Translational Research & Clinical Interventions published by Wiley Periodicals, Inc. on behalf of Alzheimer's Association.Introduction PRI-002 is an orally available anti-amyloid beta (Aβ) prionic compound developed for direct disassembly of toxic Aβ oligomers relevant to Alzheimer's disease. Methods Two placebo-controlled clinical phase I trials with oral dosing of PRI-002 were conducted in healthy young subjects A single ascending dose trial (4, 12, 36, 108, or 320 mg PRI-002 or placebo) in 40 participants followed by a multiple ascending dose study with daily 160 mg PRI-002 for 14 days or 320 mg for 28 days in 24 participants. The main objectives were safety, tolerability, and evaluation of pharmacokinetic (PK) parameters. Results PRI-002 was safe and well tolerated after single and multiple oral administration up to the highest doses. PRI-002 was absorbed rapidly and drug exposure increased proportional to dose. During repeated daily administration, the drug accumulated by a factor of about three. Steady-state conditions were reached after 1 to 2 weeks. Conclusions The safety and PK results encourage further clinical development of PRI-002. © 2020 The Authors. Alzheimer's & Dementia Translational Research & Clinical Interventions published by Wiley Periodicals, Inc. on behalf of Alzheimer's Association.Introduction Post-stroke neurocognitive disorder (NCD) is common; prevalence varies between studies, partially related to lack of consensus on how to identify cases. The aim was to compare the prevalence of post-stroke NCD using only cognitive assessment (model A), DSM-5 criteria (model B), and the Global Deterioration Scale (model C) and to determine agreement among the three models. Methods In the Norwegian Cognitive Impairment After Stroke study, 599 patients were assessed 3 months after suffering a stroke. Results The prevalence of mild NCD varied from 174 (29%) in model B to 83 (14%) in model C; prevalence of major NCD varied from 249 (42%) in model A to 68 (11%) in model C. Cohen's kappa and Cohen's quadratic weighted kappa showed fair to very good agreement among models; the poorest agreement was found for identification of mild NCD. Discussion The findings indicate a need for international harmonization to classify post-stroke NCD. © 2020 The Authors. Alzheimer's & Dementia Translational Research & Clinical Interventions published by Wiley Periodicals, Inc. on behalf of Alzheimer's Association.Objective To test the hypothesis that among cognitively healthy individuals, distinct groups exist in terms of amyloid and phosphorylated-tau accumulation rates; that if rapid accumulator groups exist, their membership can be predicted by Alzheimer's disease (AD) risk factors, and that time points of significant increase in AD protein accumulation will be evident. Methods The analysis reports data from 263 individuals from the BIOCARD and 184 individuals from the Baltimore Longitudinal Study of Aging with repeated cerebrospinal fluid (CSF) and positron emission tomography (PET) sampling, respectively. We used latent class mixed-effect models to identify distinct classes of amyloid (CSF and PET) and p-Tau (CSF) accumulation rates and generalized additive modeling to investigate non-linear changes to AD biomarkers. Results For both amyloid and p-Tau latent class models we confirmed the existence of two separate classes accumulators and non-accumulators. The accumulator and non-accumulator groups differed significantly in terms of baseline AD protein levels and slope of change.

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