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Background: Nonverbal cognitive training for aphasia has gained popularity. Prior research has found that cognitive status correlates with language function. Objective: To determine whether nonverbal computer-assisted executive control training (CAET) to improve cognitive status affects language performance in patients with aphasia (PWA) and executive dysfunction. Design: A single blind randomized trial. Setting: Department of Rehabilitation, Affiliated Hospital of Xuzhou Medical University. Participants: A total of 68 individuals were randomized, underwent treatment and were included in the analysis (CAET group, n = 33; control group, n = 35). Interventions: The experimental group was treated with 4 weeks of traditional speech and language therapy (SLT) combined with CAET. The control group underwent SLT only. Main Outcome Measures: Western Aphasia Battery [WAB]) with executive dysfunction (as assessed by the verbal fluency test [VFT], the Proverbs Test, the Tower of London Test [TLT], the Stroop Color and Word Test [SCWT], and the Trail Making Test [TMT]). Results: Differences between pre- and posttreatment language outcomes except oral naming (group x time, p = .236) were significantly greater in the experimental group compared with the control group: spontaneous speech (group x time, p = .026), auditory comprehension (group x time, p < .001), speech repetition (group x time, p = .001), and aphasia quotient (AQ; group x time, p < .001). A similar effect was observed for cognitive function such as Trial Making Test (TMT)-A (group x time, p = .006), TMT-B (group x time, p = .005), and verbal fluency test (VFT-V; group x time, p = .018). Conclusion: The study demonstrates that CAET combined with SLT can yield favorable language outcomes for PWA, especially improvements in auditory comprehension and AQ. CAET combined with SLT generates benefits in both cognitive function and language performance. [ABSTRACT FROM AUTHOR]

Cholinergic deficiency has been implicated in the pathogenesis of vascular cognitive impairment (VCI), but the extent of involvement and underlying mechanism remain unclear. In this study, targeting the early stage of VCI, we determined regional atrophy within the basal forebrain and deficiency in cholinergic pathways in 25 patients with vascular cognitive impairment no dementia (VCIND) compared to 24 healthy elderly subjects. By applying stereotaxic cytoarchitectonic maps of the nucleus basalis of Meynert (NbM), no significant atrophy was identified in VCIND. Using probabilistic tractography analysis, our study tracked the two major white matter tracks which map to cholinergic pathways. We identified significantly lower fractional anisotropy (FA) in VCIND. Mediation analysis demonstrated that FA in the tracked pathways could fully account for the executive dysfunction, and partly mediate the memory and global cognition impairment. Our study suggests that the fibers mapped to the cholinergic pathways, but not the NbM, are significantly impaired in VCIND. MRI-based in vivo tracking of cholinergic pathways together with NbM measurement may become a valuable in vivo marker for evaluating the cholinergic system in cognitive disorders. [ABSTRACT FROM AUTHOR]

Background: Vascular cognitive impairment, no dementia (VCIND) refers to cognitive deficits associated with underlying vascular causes that fall short of a dementia diagnosis. There is currently no treatment for VCIND. Computerized cognitive training, which has significantly improved cognitive function in healthy older adults and patients with cognitive impairment has not yet been applied to VCIND.Methods/design: The proposed study is a three-center, double-blinded, randomized controlled trial that will include 60 patients with VCIND. The patients will be randomized to either a training or a control group. The intervention is internet-based cognitive training performed for 30 min over 35 sessions. Neuropsychological assessment and functional and structural MRI will be performed before and after 7 weeks training. Primary outcomes are global cognitive function and executive function. Secondary outcome measures are neuroplasticity changes measured by functional and structural MRI.Discussion: Applying an internet-based, multi-domain, adaptive program, this study aims to assess whether cognitive training improves cognitive abilities and neural plasticity in patients with subcortical VCIND. In addition to the comprehensive assessment of the participants by neuropsychological tests, cerebrovascular risk factors and apolipoprotein E genotyping, neuroplasticity will be used as an evaluation outcome in this study for, to our knowledge, the first time. The combination of functional and structural MRI and neuropsychological tests will have strong sensitivity in evaluating the effects of cognitive training and will also reveal the underlying mechanisms at work.Trial Registration: ClinicalTrials.gov NCT02640716 . Retrospectively registered on 21 December 2015. [ABSTRACT FROM AUTHOR]

Task-induced deactivations within the brain's default mode network (DMN) are thought to reflect suppression of endogenous thought processes to support exogenous goaldirected task processes. Older adults are known to show reductions in deactivation of the DMN compared to younger adults. However, little is understood about the mechanisms contributing to functional dysregulation of the DMN in aging. Here, we explored the relationships between functional modulation of the DMN and age, task performance and white matter (WM) microstructure. Participants were 117 adults ranging from 25 to 83 years old who completed an fMRI task switching paradigm, including easy (single) and difficult (mixed) conditions, and underwent diffusion tensor imaging (DTI). The fMRI results revealed an age by condition interaction (β = −0.13, t = −3.16, p = 0.002) such that increasing age affected deactivation magnitude during the mixed condition (β = −0.29, t = −3.24 p = 0.002) but not the single condition (p = 0.58). Additionally, there was a WM by condition interaction (β = 0.10, t = 2.33, p = 0.02) such that decreasing WM microstructure affected deactivation magnitude during the mixed condition (β = 0.30, t = 3.42 p = 0.001) but not the single condition (p = 0.17). Critically, mediation analyses indicated that age-related reductions in WM microstructure accounted for the relationship between age and DMN deactivation in the more difficult mixed condition. These findings suggest that age-related declines in anatomical connectivity between DMN regions contribute to functional dysregulation within the DMN in older adults. [ABSTRACT FROM AUTHOR]