6 research outputs found

    Brain age as a biomarker for pathological versus healthy ageing – a REMEMBER study

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    Objectives: This study aimed to evaluate the potential clinical value of a new brain age prediction model as a single interpretable variable representing the condition of our brain. Among many clinical use cases, brain age could be a novel outcome measure to assess the preventive effect of life-style interventions. Methods: The REMEMBER study population (N = 742) consisted of cognitively healthy (HC,N = 91), subjective cognitive decline (SCD,N = 65), mild cognitive impairment (MCI,N = 319) and AD dementia (ADD,N = 267) subjects. Automated brain volumetry of global, cortical, and subcortical brain structures computed by the CE-labeled and FDA-cleared software icobrain dm (dementia) was retrospectively extracted from T1-weighted MRI sequences that were acquired during clinical routine at participating memory clinics from the Belgian Dementia Council. The volumetric features, along with sex, were combined into a weighted sum using a linear model, and were used to predict ‘brain age’ and ‘brain predicted age difference’ (BPAD = brain age–chronological age) for every subject. Results: MCI and ADD patients showed an increased brain age compared to their chronological age. Overall, brain age outperformed BPAD and chronological age in terms of classification accuracy across the AD spectrum. There was a weak-to-moderate correlation between total MMSE score and both brain age (r = -0.38,p < .001) and BPAD (r = -0.26,p < .001). Noticeable trends, but no significant correlations, were found between BPAD and incidence of conversion from MCI to ADD, nor between BPAD and conversion time from MCI to ADD. BPAD was increased in heavy alcohol drinkers compared to non-/sporadic (p = .014) and moderate (p = .040) drinkers. Conclusions: Brain age and associated BPAD have the potential to serve as indicators for, and to evaluate the impact of lifestyle modifications or interventions on, brain health

    EEG in Silent Small Vessel Disease:sLORETA Mapping Reveals Cortical Sources of Vascular Cognitive Impairment No Dementia in the Default Mode Network

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    <p>Introduction: Vascular cognitive impairment, no dementia (vCIND) is a prevalent and potentially preventable disorder. Clinical presof the small vessel subcortical subtype may be insidious and difficult to diagnose in the initial stage. We investigated electroencephalographic sources of subcortical vCIND in comparison to amnesic multidomain mild cognitive impairment (amdMCI) to determine the additional diagnostic value of quantitative electroencephalograhy (EEG) in this setting.</p><p>Methods: Fifty-seven community residing patients with an uneventful central neurological history and first presentation of cognitive decline without dementia were included, 35 patients were diagnosed with vCIND and 22 with amdMCI. A cognitive control group, deliberately recruited from a cerebrovascular impaired cohort, consisted of cognitively healthy participants who experienced a fully recovered first ever transient ischemic attack (TIA) without clinical or magnetic resonance imaging evidence of stroke. From standard EEGs, the differences in standardized low-resolution brain electromagnetic tomography (sLORETA) sources were determined for the discrete frequency ranges 1-4 (delta), 4-8 (theta), 8-10.5 (alpha1), 10.5-13 (alpha2), 13-22 (beta1), and 22-30 (beta2) Hz.</p><p>Results: In vCIND, a statistically significant decrease in parietooccipital alpha1 relative power current density compared with TIA and mild cognitive impairment patients was found. There was a significant decrease in frontal and parietooccipital beta1 relative power current density in vCIND compared with TIA patients. A significant increase in (pre) frontal delta relative power current density in vCIND compared with amdMCI was found as well. In amdMCI, delta relative power current density was significantly increased in the core limbic system.</p><p>Discussion: Cortical sources of abnormal EEG activity in regions implicated in the default mode network are revealed by sLORETA at an early stage in vascular cognitive impairment. Mapping of parietooccipital alpha1, frontoparietooccipital beta1 and (pre) frontal delta loci in vCIND may reflect early executive and visuospatial dysfunction in this cohort. Standard EEG with sLORETA mapping might be an additional, noninvasive, and cost-effective tool in the diagnostic workup of patients presenting with a cognitive decline.</p>

    Subcortical Vascular Cognitive Impairment, No Dementia:EEG Global Power Independently Predicts Vascular Impairment and Brain Symmetry Index Reflects Severity of Cognitive Decline

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    Background and Purpose:Vascular cognitive impairment, no dementia (vCIND) is a prevalent and potentially preventable disorder. Clinical presentation of the small-vessel subcortical subtype may be insidious, and differential difficulties can arise with mild cognitive impairment. We investigated EEG parameters in subcortical vCIND in comparison with amnestic multidomain mild cognitive impairment to determine the additional diagnostic value of quantitative EEG in this setting.Methods:Fifty-seven community-residing patients with an uneventful central neurologic history and first presentation of cognitive decline without dementia were included. Neuropsychological test results were correlated with EEG parameters. Predictive values for vCIND and amnestic multidomain mild cognitive impairment were calculated using receiver operating characteristic curves and logistic regression modeling.Results:Vascular cognitive impairment, no dementia and amnestic multidomain mild cognitive impairment differed with regard to the EEG (delta + theta)/(alpha + beta) ratio (DTABR) and pairwise derived brain symmetry index. We found statistically significant correlations between pairwise derived brain symmetry index and immediate verbal memory, immediate global memory, verbal recognition, working memory, and mean memory score in vCIND. Verbal fluency (odds ratio: 1.54, 95% confidence interval: 1.04-2.28, P = 0.033) and (delta + theta)/(alpha + beta) ratio (odds ratio: 2.28, 95% confidence interval: 1.06-4.94, P = 0.036) emerged as independent diagnostic predictors for vCIND with an overall correct classification rate of 95.0%.Conclusion:Our data indicate that EEG is of additional value in the differential diagnosis and follow-up of patients presenting with cognitive decline. These findings may have an impact on memory care

    Brain age as a biomarker for pathological versus healthy ageing – a REMEMBER study

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    Objectives: This study aimed to evaluate the potential clinical value of a new brain age prediction model as a single interpretable variable representing the condition of our brain. Among many clinical use cases, brain age could be a novel outcome measure to assess the preventive effect of life-style interventions. Methods: The REMEMBER study population (N = 742) consisted of cognitively healthy (HC,N = 91), subjective cognitive decline (SCD,N = 65), mild cognitive impairment (MCI,N = 319) and AD dementia (ADD,N = 267) subjects. Automated brain volumetry of global, cortical, and subcortical brain structures computed by the CE-labeled and FDA-cleared software icobrain dm (dementia) was retrospectively extracted from T1-weighted MRI sequences that were acquired during clinical routine at participating memory clinics from the Belgian Dementia Council. The volumetric features, along with sex, were combined into a weighted sum using a linear model, and were used to predict ‘brain age’ and ‘brain predicted age difference’ (BPAD = brain age–chronological age) for every subject. Results: MCI and ADD patients showed an increased brain age compared to their chronological age. Overall, brain age outperformed BPAD and chronological age in terms of classification accuracy across the AD spectrum. There was a weak-to-moderate correlation between total MMSE score and both brain age (r = -0.38,p <.001) and BPAD (r = -0.26,p <.001). Noticeable trends, but no significant correlations, were found between BPAD and incidence of conversion from MCI to ADD, nor between BPAD and conversion time from MCI to ADD. BPAD was increased in heavy alcohol drinkers compared to non-/sporadic (p =.014) and moderate (p =.040) drinkers. Conclusions: Brain age and associated BPAD have the potential to serve as indicators for, and to evaluate the impact of lifestyle modifications or interventions on, brain health.SCOPUS: ar.jinfo:eu-repo/semantics/publishe
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