scholarly journals Memory enhancement by multidomain group cognitive training in patients with Parkinson’s disease and mild cognitive impairment: long-term effects of a multicenter randomized controlled trial

Author(s):  
Nele Schmidt ◽  
Inken Tödt ◽  
Daniela Berg ◽  
Christian Schlenstedt ◽  
Ann-Kristin Folkerts ◽  
...  

Abstract Background Meta-analyses indicate positive effects of cognitive training (CT) in patients with Parkinson’s disease (PD), however, most previous studies had small sample sizes and did not evaluate long-term follow-up. Therefore, a multicenter randomized controlled, single-blinded trial (Train-ParC study) was conducted to examine CT effects in PD patients with mild cognitive impairment (PD-MCI). Immediately after CT, an enhancement of executive functions was demonstrated. Here, we present the long-term results 6 and 12 months after CT. Methods At baseline, 64 PD-MCI patients were randomized to a multidomain CT group (n = 33) or to a low-intensity physical activity training control group (PT) (n = 31). Both interventions included 90 min training sessions twice a week for 6 weeks. 54 patients completed the 6 months (CT: n = 28, PT: n = 26) and 49 patients the 12 months follow-up assessment (CT: n = 25, PT: n = 24). Primary study outcomes were memory and executive functioning composite scores. Mixed repeated measures ANOVAs, post-hoc t tests and multiple regression analyses were conducted. Results We found a significant time x group interaction effect for the memory composite score (p = 0.006, η2 = 0.214), but not for the executive composite score (p = 0.967, η2 = 0.002). Post-hoc t tests revealed significant verbal and nonverbal memory improvements from pre-intervention to 6 months, but not to 12 months follow-up assessment in the CT group. No significant predictors were found for predicting memory improvement after CT. Conclusions This study provides Class 1 evidence that multidomain CT enhances memory functioning in PD-MCI after 6 months but not after 12 months, whereas executive functioning did not change in the long-term. Clinical trial registration German Clinical Trials Register (ID: DRKS00010186), 21.3.2016 (The study registration is outlined as retrospective due to an administrative delay. The first patient was enrolled three months after the registration process was started. A formal confirmation of this process from the German Clinical Trials Register can be obtained from the authors.)

2010 ◽  
Vol 6 ◽  
pp. S493-S493
Author(s):  
Galeno J. Rojas ◽  
Veronica Villar ◽  
Monica Iturry ◽  
Leonardo Bartoloni ◽  
Paula Harris ◽  
...  

2021 ◽  
pp. 135245852110002
Author(s):  
Bruce AC Cree ◽  
Jeffrey A Cohen ◽  
Anthony T Reder ◽  
Davorka Tomic ◽  
Diego Silva ◽  
...  

Background: Disease-modifying therapies (DMTs) can reduce the risk of disability worsening in patients with relapsing forms of multiple sclerosis (RMS). High-efficacy DMTs can lead to confirmed or sustained disability improvement (CDI and SDI). Objective and Methods: Post hoc analyses of data from the TRANSFORMS, FREEDOMS, and FREEDOMS II trials and their extensions assessed the effects of fingolimod (0.5–1.25 mg/day) on stabilizing or improving disability over ⩽8 years in participants with RMS. CDI and SDI rates were compared between participants initially randomized to fingolimod, interferon (IFNβ-1a), or placebo. Results: At 8 years’ follow-up in TRANSFORMS, 35.1% (95% confidence interval [CI], 28.2%–43.1%) of assessed participants in the IFNβ-1a–fingolimod switch group and 41.9% (36.6%–47.6%) on continuous fingolimod experienced CDI; disability did not worsen in approximately 70%. Similar results were seen in the combined FREEDOMS population. Proportionally fewer TRANSFORMS participants achieved SDI in the IFNβ-1a–fingolimod switch group than on continuous fingolimod (5.4% [3.0%–9.5%] vs 14.2% [10.8%–18.4%], p = 0.01). Conclusion: CDI and SDI are outcomes of interest for clinical trials and for long-term follow-up of participants with RMS. Monitoring CDI and SDI in addition to disability worsening may facilitate understanding of the therapeutic benefit of RMS treatments.


2020 ◽  
Vol 32 (S1) ◽  
pp. 91-91

AUTHORS:Kerstin Johansson, Karolina Thömkvist, Ingmar Skoog and Sacuiu SF* (*presenter)OBJECTIVE:To determine the effects of electroconvulsive therapy (ECT) in major depression in relation to the development of dementia during long-term follow-up.METHOD:In an observational clinical prospective study of consecutive patients 70 years and older diagnosed with major depression at baseline 2000-2004 (n=1090), who were free of dementia and received antidepressant treatment, with or without ECT, we sought to determine if cognitive decline (mild cognitive impairment and dementia) during 15 -year follow-up was associated with receiving ECT at baseline. The control group was selected among the participants in the Gothenburg H70 Birth Cohort Studies matched by age group and sex 1:1.RESULTS:Among patients with affective syndromes 7% received ECT. During follow-up, 157 patients were diagnosed with dementia, equal proportions among those who received ECT (14.5%) and those who did not receive ECT (14.5%). The relation between ECT and cognitive decline remained non-significant irrespective antidepressive medication or presence of mild cognitive impairment at baseline.CONCLUSION:Preliminary results indicate that ECT was not associated with the development of cognitive decline in the long-term in a hospital-based cohort of 70+ year-olds. The results remain to verify against controls from a representative community sample.


2019 ◽  
Author(s):  
Danni Li ◽  
Michelle M Mielke ◽  
W Robert Bell ◽  
Cavan Reilly ◽  
Lin Zhang ◽  
...  

Abstract Background: Alzheimer’s disease (AD) is an epidemic with tremendous public health impacts because there are currently no disease-modifying therapeutics. Randomized controlled trials (RCTs) for prevention of AD dementia often use clinical endpoints that take years to manifest (e.g., cognition) or surrogate endpoints that are costly or invasive (e.g., magnetic resonance imaging [MRI]). Blood biomarkers represent a clinically applicable alternative surrogate endpoint for RCTs that would be both cost-effective and minimally invasive, but little is known about their value as surrogate endpoints for treatment responses in the prevention of AD dementia. Methods: The objective of this study is to investigate blood neuropathological, neurodegenerative, and neurotrophic biomarkers as surrogate endpoints for treatment responses to 3 interventions in older adults with amnestic mild cognitive impairment (aMCI, a prodromal stage of AD): aerobic exercise; cognitive training; and combined aerobic exercise and cognitive training (ACT). We chose these three sets of biomarkers for their unique mechanistic associations with AD pathology, neurodegeneration and neurogenesis. This study is built on the ACT Trial (1R01AG055469), a single-blinded, multi-site, 2×2 factorial Phase II RCT that examines the synergistic effects of a 6-month ACT intervention on cognition and MRI biomarkers (AD-signature cortical thickness and hippocampal volume) (n=128). In this ACT Trial Blood Biomarkers Study, we will enroll 120 ACT Trial aMCI participants and measure blood biomarkers at baseline, 3, 6, 12 and 18 months. The goals are to: (1) Determine the effect of interventions on blood biomarkers over 6 months; (2) Evaluate blood biomarkers as surrogate endpoints for predicting cognitive responses to interventions over 18 months; and (3; exploratory) Examine blood biomarkers as surrogate endpoints for predicting brain MRI biomarker responses to interventions over 18 months. Discussion: This study aims to identify new blood biomarkers that can track cognitive decline or AD-related brain atrophy among aMCI patients subjected to a regimen of aerobic exercise and cognitive training. Findings from this study will drive the further use of blood biomarkers in developing effective prevention and treatment strategies for AD dementia. Trial registration number: This study is an ancillary study of the ACT Trial which was registered with ClinicalTrials.gov, NCT03313895.


Sign in / Sign up

Export Citation Format

Share Document