Background: Late-life depression (LLD) is characterized by differences in resting state functional connectivity within and between intrinsic functional networks. This study examined whether clinical improvement to antidepressant medications is associated with pre-randomization functional connectivity in intrinsic brain networks.
Methods: Participants were 95 elders aged 60 years or older with major depressive disorder. After clinical assessments and baseline MRI, participants were randomized to escitalopram or placebo with a two-to-one allocation for 8 weeks. Non-remitting participants subsequently entered an 8-week trial of open-label bupropion. The main clinical outcome was depression severity measured by MADRS. Resting state functional connectivity was measured between key seeds in the default mode (DMN), cognitive control, and limbic networks.
Results: In primary analyses of blinded data, lower post-treatment MADRS score was associated with higher resting connectivity between: (a) posterior cingulate cortex (PCC) and left medial prefrontal cortex; (b) PCC and subgenual anterior cingulate cortex (ACC); (c) right medial PFC and subgenual ACC; (d) right orbitofrontal cortex and left hippocampus. Lower post-treatment MADRS was further associated with lower connectivity between: (e) the right orbitofrontal cortex and left amygdala; and (f) left dorsolateral PFC and left dorsal ACC. Secondary analyses associated mood improvement on escitalopram with anterior DMN hub connectivity. Exploratory analyses of the bupropion open-label trial associated improvement with subgenual ACC, frontal, and amygdala connectivity.
Conclusions: Response to antidepressants in LLD is related to connectivity in the DMN, cognitive control and limbic networks. Future work should focus on clinical markers of network connectivity informing prognosis.
Registration: ClinicalTrials.gov NCT02332291.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10250562 | PMC |
http://dx.doi.org/10.1017/S0033291722003579 | DOI Listing |
Cureus
December 2024
Research Team for Human Care, Tokyo Metropolitan Institute for Geriatrics and Gerontology, Tokyo, JPN.
Purpose Muscle atrophy progresses with age. The motor function may be estimated by measuring the muscle mass; however, if muscle quality deteriorates due to an increase in connective tissue within the muscle, a decline in motor function may be missed by measuring muscle mass alone. Therefore, it is important to understand the relationship between muscle mass, muscle quality, and motor function.
View Article and Find Full Text PDFMediterr J Rheumatol
December 2024
Department of Pulmonary Medicine, Kalinga Institute of Medical Sciences, KIIT University, Bhubaneswar, Odisha, India.
Background: Sarcopenia, a progressive loss of skeletal muscle strength and mass, can lead to decreased quality of life, physical disability, and mortality. Early identification of sarcopenia is crucial in limiting morbidity and mortality in connective tissue disease associated interstitial lung diseases (CTDILD) patients.
Objective: The objectives of this study are to determine the prevalence of sarcopenia in CTD-ILD patients and to correlate the severity of sarcopenia with pulmonary function tests, spirometry, and 6-minute walk test (6MWT).
Neural Regen Res
January 2025
The Ritchie Centre, Hudson Institute of Medical Research, Melbourne, VIC, Australia.
Perinatal exposure to infection/inflammation is highly associated with neural injury, and subsequent impaired cortical growth, disturbances in neuronal connectivity, and impaired neurodevelopment. However, our understanding of the pathophysiological substrate underpinning these changes in brain structure and function is limited. The objective of this review is to summarize the growing evidence from animal trials and human cohort studies that suggest exposure to infection/ inflammation during the perinatal period promotes regional impairments in neuronal maturation and function, including loss of high-frequency electroencephalographic activity, and reduced growth and arborization of cortical dendrites and dendritic spines resulting in reduced cortical volume.
View Article and Find Full Text PDFNeural Regen Res
January 2025
Ajou University School of Medicine, Department of Brain Science, Suwon, Republic of Korea.
Spinal cord injury results in permanent loss of neurological functions due to severance of neural networks. Transplantation of neural stem cells holds promise to repair disrupted connections. Yet, ensuring the survival and integration of neural stem cells into the host neural circuit remains a formidable challenge.
View Article and Find Full Text PDFNeural Regen Res
January 2025
School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
After spinal cord injury, impairment of the sensorimotor circuit can lead to dysfunction in the motor, sensory, proprioceptive, and autonomic nervous systems. Functional recovery is often hindered by constraints on the timing of interventions, combined with the limitations of current methods. To address these challenges, various techniques have been developed to aid in the repair and reconstruction of neural circuits at different stages of injury.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!