Background: We examined the association of cognitive vulnerability to depression with changes in homogeneous measures of depressive symptoms.
Methods: Baseline and 1-year follow-up data were obtained from 2981 participants of the Netherlands study of depression and anxiety. Multivariate regression analyses were carried out on cognitive reactivity, locus of control and implicit and explicit self-depressive associations in combination with negative life events. The purpose of this analysis was to predict changes on the mood/cognition and anxiety/arousal subscales of the inventory of depressive symptomatology - self report.
Results: Cognitive reactivity, locus of control and explicit self-depressive associations were independently associated with changes in depressive symptoms after adjustment for covariates and baseline severity (all p<0.01). Negative life-events interacted with cognitive vulnerability to depression to predict depressive symptoms. Locus of control (b1=0.16, SE=0.02, η(2)=0.01; b2=0.10, SE=0.02, η(2)=0.004, F=8.69, p<0.01) and explicit self-depressive associations (b1=0.10, SE=0.03, η(2)=0.02; b2=0.02, SE=0.04, F=7.50, p<0.01) were more strongly associated with the cognitive (b1) than the somatic (b2) symptom dimension of depression.
Limitations: The study sample is over-inclusive of depressed patients. Therefore it might be problematic generalizing the findings to the general population.
Conclusion: Cognitive etiological factors may play a role in a "cognitive" subtype of depression. The findings strengthen the notion that homogeneous measures of depressive symptoms enable a greater degree of discrimination between subtypes than a multidimensional conception of depression.
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http://dx.doi.org/10.1016/j.jad.2013.05.057 | DOI Listing |
Aging Clin Exp Res
January 2025
Instituto de Neurociencias del Principado de Asturias (INEUROPA), University of Oviedo, Oviedo, 33003, Spain.
Background: The presence of frailty is common in people with Parkinson's disease, as is cognitive dysfunction. Previous research on frailty has focused on the physical aspects of the pathology.
Aims: To analyze the relationship between frailty and cognitive impairment in patients with Parkinson's disease and to know which disease characteristics are associated with frailty.
Alzheimers Dement
December 2024
Albany Medical College, Albany, NY, USA.
Background: Stress is a common modifiable risk factor for AD, which increases dementia risk 2-fold. During the stress response, the hypothalamic-pituitary adrenal (HPA) axis is activated which stimulates the release of stress hormones called glucocorticoids into the blood stream. Studies on early-life stress have shown a glucocorticoid dependent vulnerability towards late-life inflammation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Background: Women are disproportionately affected by Alzheimer's disease (AD) and exhibit greater AD neuropathology than men. Women possess two X chromosomes, with one randomly silenced across each cell for dosage compensation. X chromosome inactivation (XCI) is not complete, and XCI-escaping genes provide a promising avenue of discovery for biological pathways driving sex-specific AD risk.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Mount Sinai Center for Transformative Disease Modeling, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease that inflicts the elderly worldwide. Recent studies revealed the association of abnormal methylomic alterations in AD. However, a systematic and comprehensive study is needed to investigate the effects of methylomic changes on the molecular networks underpinning AD, in particular, in brain regions most vulnerable to AD neuropathology.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Beth Israel Deaconess Medical Center, Boston, MA, USA.
Background: A significant proportion of individuals preserve cognitive function despite meeting neuropathological criteria for Alzheimer's disease (AD) at autopsy, known as cognitive resilience. We aimed to define the molecular and cellular signatures of cognitive resilience against AD.
Method: We integrated multi-modal data from the Religious Order Study and Memory and Aging Project (ROSMAP), including bulk (n = 631) and multi-regional single nucleus (n = 48) RNA sequencing.
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