18 research outputs found

    Symptoms of anxiety and depression are related to cardiovascular responses to active, but not passive, coping tasks

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    Objective: Anxiety and depression have been linked to blunted blood pressure (BP) and heart rate (HR) reactions to mental stress tests; however, most studies have not included indices of underlying hemodynamics nor multiple stress tasks. This study sought to examine the relationships of anxiety and depression with hemodynamic responses to acute active and passive coping tasks. Methods: A total of 104 participants completed the Hospital Anxiety and Depression Scales and mental arithmetic, speech, and cold pressor tasks while BP, HR, total peripheral resistance, and cardiac output (CO) were assessed. Results: After adjustment for traditional risk factors and baseline cardiovascular activity, depression scores were negatively associated with systolic BP, HR, and CO responses to the mental arithmetic task, while anxiety scores were inversely related to the systolic BP response to mental arithmetic. Conclusion: High anxiety or depression scores appear to be associated with blunted cardiac reactions to mental arithmetic (an active coping task), but not to the cold pressor test or speech tasks. Future research should further examine potential mechanisms and longitudinal pathways relating depression and anxiety to cardiovascular reactivity

    Understanding the somatic consequences of depression: biological mechanisms and the role of depression symptom profile

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    An Exploratory Study of Sleep-Wake Differences of Autonomic Activity in Patients with Mild Cognitive Impairment: The Role of Melatonin as a Modulating Factor

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    Carolina Abulafia,1,2 MarĂ­a F Vidal,3 Natividad Olivar,4 Andrea Odzak,5 Ignacio Brusco,4– 6 Salvador M Guinjoan,7 Daniel P Cardinali,8 Daniel E Vigo1,9 1Laboratory of Chronophysiology, Institute for Biomedical Research (BIOMED), Pontifical Catholic University of Argentina (UCA) and CONICET, Buenos Aires, Argentina; 2Facultad de PsicologĂ­a, Universidad de Buenos Aires, Buenos Aires, Argentina; 3Servicio de PsiquiatrĂ­a, Departamento de NeurologĂ­a, Fleni, Buenos Aires, Argentina; 4Hospital de ClĂ­nicas “JosĂ© de San MartĂ­n”, Universidad de Buenos Aires, Buenos Aires, Argentina; 5Servicio de ClĂ­nica MĂ©dica, Hospital Argerich, Buenos Aires, Argentina; 6CONICET, Buenos Aires, Argentina; 7Laureate Institute for Brain Research, Tulsa, OK, USA; 8Facultad de Ciencias MĂ©dicas, Universidad CatĂłlica Argentina, Buenos Aires, Argentina; 9Faculty of Psychology and Educational Sciences, Katholieke Universiteit Leuven, Leuven, BelgiumCorrespondence: Daniel E Vigo, Instituto de Investigaciones BiomĂ©dicas, Pontificia Universidad CatĂłlica Argentina, Alicia Moreau de Justo 1500, 4° piso, Buenos Aires, C1107AAZ, Argentina, Tel +54 0810-2200-822 ext 1152, Email [email protected]; [email protected]: The objective of the present study was to assess sleep-wake differences of autonomic activity in patients with mild cognitive impairment (MCI) compared to control subjects. As a post-hoc objective, we sought to evaluate the mediating effect of melatonin on this association.Patients and Methods: A total of 22 MCI patients (13 under melatonin treatment) and 12 control subjects were included in this study. Sleep-wake periods were identified by actigraphy and 24hr-heart rate variability measures were obtained to study sleep-wake autonomic activity.Results: MCI patients did not show any significant differences in sleep-wake autonomic activity when compared to control subjects. Post-hoc analyses revealed that MCI patients not taking melatonin displayed lower parasympathetic sleep-wake amplitude than controls not taking melatonin (RMSSD − 7 ± 1 vs 4 ± 4, p = 0.004). In addition, we observed that melatonin treatment was associated with greater parasympathetic activity during sleep (VLF 15.5 ± 0.1 vs 15.1 ± 0.1, p = 0.010) and in sleep-wake differences in MCI patients (VLF 0.5 ± 0.1 vs 0.2 ± 0.0, p = 0.004).Conclusion: These preliminary findings hint at a possible sleep-related parasympathetic vulnerability in patients at prodromal stages of dementia as well as a potential protective effect of exogenous melatonin in this population.Keywords: heart rate variability, actigraphy, circadian rhythms, wavelet

    Cognitive reserve and Aβ1-42 in mild cognitive impairment (Argentina-Alzheimer’s Disease Neuroimaging Initiative)

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    Paula Harris,1,2 Marcos Fernandez Suarez,1 Ezequiel I Surace,1,2 Patricio Chrem Méndez,1 María Eugenia Martín,1 María Florencia Clarens,1 Fernanda Tapajóz,1,2 Maria Julieta Russo,1 Jorge Campos,1 Salvador M Guinjoan,1,2 Gustavo Sevlever,1 Ricardo F Allegri1,2 1Instituto de Investigaciones Neurológicas, 2Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina Background: The purpose of this study was to investigate the relationship between cognitive reserve and concentration of Aβ1-42 in the cerebrospinal fluid (CSF) of patients with mild cognitive impairment, those with Alzheimer’s disease, and in control subjects. Methods: Thirty-three participants from the Argentina-Alzheimer’s Disease Neuroimaging Initiative database completed a cognitive battery, the Cognitive Reserve Questionnaire (CRQ), and an Argentinian accentuation reading test (TAP-BA) as a measure of premorbid intelligence, and underwent lumbar puncture for CSF biomarker quantification. Results: The CRQ significantly correlated with TAP-BA, education, and Aβ1-42. When considering Aβ1-42 levels, significant differences were found in CRQ scores; higher levels of CSF Aβ1-42 were associated with higher CRQ scores. Conclusion: Reduced Aβ1-42 in CSF is considered as evidence of amyloid deposition in the brain. Previous results suggest that individuals with higher education, higher occupational attainment, and participation in leisure activities (cognitive reserve) have a reduced risk of developing Alzheimer’s disease. Our results support the notion that enhanced neural activity has a protective role in mild cognitive impairment, as evidenced by higher CSF Aβ1-42 levels in individuals with more cognitive reserve. Keywords: amyloid, biomarkers, cerebrospinal fluid, Alzheimer’s disease&nbsp
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