Artifacts in fMRI data, primarily those related to motion and physiological sources, negatively impact the functional signal-to-noise ratio in fMRI studies, even after conventional fMRI preprocessing. Independent component analysis’ demonstrated capacity to separate sources of neural signal, structured noise, and random noise into separate components might be utilized in improved procedures to remove artifacts from fMRI data. Such procedures require a method for labeling independent components (ICs) as representing artifacts to be removed or neural signals of interest to be spared. Visual inspection is often considered an accurate method for such labeling as well as a standard to which automated labeling methods are compared. However, detailed descriptions of methods for visual inspection of ICs are lacking in the literature. Here we describe the details of, and the rationale for, an operationalized fMRI data denoising procedure that involves visual inspection of ICs (96% inter-rater agreement). We estimate that dozens of subjects/sessions can be processed within a few hours using the described method of visual inspection. Our hope is that continued scientific discussion of and testing of visual inspection methods will lead to the development of improved, cost-effective fMRI denoising procedures.
Background A large body of research has focused on “mediating mechanisms” and predisposing brain abnormalities to geriatric depression, but little is known about its etiology. This paper examines whether age-related and comorbid disease-related immune deregulation is an etiologic contributor to geriatric depression. Methods This article reviews findings on neuroinflammation during the aging process and depression as well as studies of anti-inflammatory actions of classical antidepressants and antidepressant actions of anti-inflammatory agents. Results Aging results in increased peripheral immune responses, impaired peripheral-CNS immune communication, and a shift of the CNS into a pro-inflammatory state. These exaggerated and prolonged immune responses may lead to changes in the function of emotional and cognitive networks pertinent to geriatric depression and to behavioral changes reminiscent of the depressive and cognitive symptoms of geriatric depression. Some antidepressants may reduce the expression of inflammation markers. Limited data suggest that some anti-inflammatory agents may have antidepressant properties. Conclusions A synthesis of available findings suggests that aging-related and comorbid disease-related inflammatory processes may promote changes in the neural systems predisposing to geriatric depression or facilitating metabolic changes that mediate depressive syndromes. The “inflammation hypothesis” in geriatric depression cannot be tested in its entirety, but it can lead to testable hypotheses and data on mechanisms by which inflammatory processes promote geriatric depression. The significance of such an effort is that it may lead to a novel treatment development model bringing to bear recent advances of anti-inflammatory pharmacology to the treatment of depressed elderly patients.
Cognitive impairment in late life depression is prevalent, disabling, and heterogeneous. Although mild cognitive impairment in depression does not usually progress to dementia, accurate assessment of cognition is vital to prognosis and treatment planning. For example, executive dysfunction often accompanies late-life depression, influences performance across cognitive domains, and is associated with poor antidepressant treatment outcomes. Here, we review how assessment can capture dysfunction across cognitive domains, and discuss cognitive trajectories frequently observed in late-life depression in the context of the neurobiology of this disorder. Furthermore we review the efficacy of a sample of interventions tailored to specific cognitive profiles.
BACKGROUND This study tested the hypothesis that use of semantic organizational strategy in approaching the Mattis Dementia Rating Scale (MDRS) Complex Verbal Initiation Perseveration (I/P) task, a test of semantic fluency, is the function specifically associated with remission of late-life depression. METHOD 70 elders with major depression participated in a 12-week escitalopram treatment trial. Neuropsychological performance was assessed at baseline after a 2-week drug washout period. Patients with a Hamilton Depression Rating Scale Score less than or equal to 7 for two consecutive weeks and who no longer met DSM-IV criteria were considered to be remitted. Cox proportional hazards survival analysis was used to examine the relationship between subtests of the I/P, other neuropsychological domains and remission rate. Participants’ performance on the CV I/P was coded for perseverations, and use of semantic strategy. RESULTS The relationship of performance on the Complex Verbal I/P and remission rate was significant. No other subtest of the MDRS I/P evidenced this association. There was no significant relationship of speed, confrontation naming, verbal memory or perseveration with remission rate. Remitters’ use of verbal strategy was significantly greater than non-remitters. CONCLUSIONS Geriatric depressed patients who showed decrements in performance on a semantic fluency task showed poorer remission rates than those who showed adequate performance on this measure. Executive impairment in verbal strategy explained performance. This finding supports the concept that executive functioning exerts a “top down” effect on other basic cognitive processes, perhaps as a result of frontostriatal network dysfunction implicated in geriatric depression.
Executive dysfunction (ED) in geriatric depression (GD) is common, predicts poor clinical outcomes and often persists despite remission of symptoms. Here we develop a neuroplasticity-based computerized cognitive remediation treatment (CCR-GD) to target ED in GD. Our assumption is that remediation of these deficits may modulate the underlying brain network abnormalities shared by executive dysfunction and depression. We compare CCR-GD to a gold standard treatment (escitalopram: 20mgs/12 weeks) in 11 treatment resistant older adults with major depression; and 33 matched historical controls. We find that 91% of participants complete CCR-GD. CCR-GD is equally as effective at reducing depressive symptoms as escitalopram but does so in 4 weeks instead of 12. In addition CCR-GD improves measures of executive function more than the escitalopram. We conclude that CCR-GD may be equally effective as escitalopram in treating GD. In addition, CCR-GD participants showed greater improvement in executive functions than historical controls treated with escitalopram.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.