Efficacy of an adjunctive computer-based cognitive training program in amnestic mild cognitive impairment and Alzheimer's disease: a single-blind, randomized clinical trial

2012 ◽  
Vol 28 (1) ◽  
pp. 91-99 ◽  
Author(s):  
Adrian Gaitán ◽  
Maite Garolera ◽  
Noemí Cerulla ◽  
Gloria Chico ◽  
Mariona Rodriguez-Querol ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Clinical Trial ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Training Program ◽  
Randomized Clinical Trial ◽  
Cognitive Training ◽  
Amnestic Mild Cognitive Impairment ◽  
Computer Based ◽  
Single Blind

Computerized Cognitive Training in Amnestic Mild Cognitive Impairment: A Randomized Clinical Trial

2021 ◽  
pp. 089198872110064
Author(s):  
Kevin Duff ◽  
Jian Ying ◽  
Kayla R. Suhrie ◽  
Bonnie C.A. Dalley ◽  
Taylor J. Atkinson ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Training ◽  
Computer Games ◽  
Brain Plasticity ◽  
Amnestic Mild Cognitive Impairment ◽  
Control Group ◽  
Computerized Cognitive Training ◽  
Secondary Outcomes

Objective: Computerized cognitive training has been successful in healthy older adults, but its efficacy has been mixed in patients with amnestic Mild Cognitive Impairment (MCI). Methods: In a randomized, placebo-controlled, double-blind, parallel clinical trial, we examined the short- and long-term efficacy of a brain-plasticity computerized cognitive training in 113 participants with amnestic MCI. Results: Immediately after 40-hours of training, participants in the active control group who played computer games performed better than those in the experimental group on the primary cognitive outcome (p = 0.02), which was an auditory memory/attention composite score. There were no group differences on 2 secondary outcomes (global cognitive composite and rating of daily functioning). After 1 year, there was no difference between the 2 groups on primary or secondary outcomes. No adverse events were noted. Conclusions: Although the experimental cognitive training program did not improve outcomes in those with MCI, the short-term effects of the control group should not be dismissed, which may alter treatment recommendations for these patients.

A Review of Computer-Based Cognitive Training for Individuals With Mild Cognitive Impairment and Alzheimer's Disease

2016 ◽  
Vol 1 (2) ◽  
pp. 47-61 ◽  
Author(s):  
Kimberly D. Mueller
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Function ◽  
Cognitive Training ◽  
Training Programs ◽  
Early Stage ◽  
Significant Evidence ◽  
Computer Based

Computer-based cognitive training programs are increasing in popularity, not only due to trends in technological advances, but also due to the intense marketing campaigns of such programs toward late-middle-aged and older adults. This article's objective is to evaluate the effectiveness of computer-based cognitive training programs in maintaining or improving cognitive function in people with mild cognitive impairment (MCI) and early-stage Alzheimer's disease (AD). Twelve databases were searched using terms related to computerized cognitive training (CCT) and MCI and Alzheimer's disease (AD). Two raters independently extracted articles using agreed-upon criteria. Due to the heterogeneity of the samples, interventions, and outcomes, data of the studies was not statistically pooled for meta-analysis. Ten studies met the inclusion criteria and the findings were summarized. All of the studies reviewed provided support that computerized cognitive interventions are feasible in people with MCI or early-stage AD. None of the studies yielded significant evidence to support the use of CCT alone for improvement or maintenance of cognitive function in people with MCI or AD. Further, no studies presented significant evidence of transfer of training to everyday skills and tasks. Recommendations for evaluating products and for areas of research need are provided.

Elucidating the risk factors for progression from amyloid-negative amnestic mild cognitive impairment to dementia

2020 ◽  
Vol 17 ◽  
Author(s):  
Hyung-Ji Kim ◽  
Jae-Hong Lee ◽  
E-nae Cheong ◽  
Sung-Eun Chung ◽  
Sungyang Jo ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Amnestic Mild Cognitive Impairment ◽  
Amyloid Pet ◽  
Clinical Progression ◽  
Amnestic Mci

Background: Amyloid PET allows for the assessment of amyloid β status in the brain, distinguishing true Alzheimer’s disease from Alzheimer’s disease-mimicking conditions. Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. However, a limited number of studies had been conducted this subpopulation in terms of clinical progression. Objective: We investigated the risk factors that could affect the progression to dementia in patients with amyloid-negative amnestic mild cognitive impairment (MCI). Methods: This study was a single-institutional, retrospective cohort study of patients over the age of 50 with amyloidnegative amnestic MCI who visited the memory clinic of Asan Medical Center with a follow-up period of more than 36 months. All participants underwent brain magnetic resonance imaging (MRI), detailed neuropsychological testing, and fluorine-18[F18]-florbetaben amyloid PET. Results: During the follow-up period, 39 of 107 patients progressed to dementia from amnestic MCI. In comparison with the stationary group, the progressed group had a more severe impairment in verbal and visual episodic memory function and hippocampal atrophy, which showed an Alzheimer’s disease-like pattern despite the lack of evidence for significant Alzheimer’s disease pathology. Voxel-based morphometric MRI analysis revealed that the progressed group had a reduced gray matter volume in the bilateral cerebellar cortices, right temporal cortex, and bilateral insular cortices. Conclusion: Considering the lack of evidence of amyloid pathology, clinical progression of these subpopulation may be caused by other neuropathologies such as TDP-43, abnormal tau or alpha synuclein that lead to neurodegeneration independent of amyloid-driven pathway. Further prospective studies incorporating biomarkers of Alzheimer’s diseasemimicking dementia are warranted.

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