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Neuroinflammatory and morphological changes in late-life depression: the NIMROD study.
L Su1, Y O Faluyi2, Y T Hong2
1Li Su, PhD, Yetunde O. Faluyi, MBChB, Department of Psychiatry, University of Cambridge, UK; Young T. Hong, PhD, Tim D. Fryer, PhD, Wolfson Brain Imaging Centre and Department of Clinical Neurosciences, University of Cambridge, UK; Elijah Mak, BA, Department of Psychiatry, University of Cambridge, UK; Silvy Gabel, MSc, Department of Psychiatry, University of Cambridge, UK and Faculty of Psychology and Neuroscience, Maastricht University, the Netherlands; Lawrence Hayes, MBBS, Soteris Soteriades, BA, Department of Psychiatry, University of Cambridge, UK; Guy B. Williams, PhD, Wolfson Brain Imaging Centre and Department of Clinical Neurosciences, University of Cambridge, UK; Robert Arnold, BSc, Department of Psychiatry, University of Cambridge, UK; Luca Passamonti, MD, Patricia Vázquez Rodríguez, MSc, Department of Clinical Neurosciences, University of Cambridge, UK, Ajenthan Surendranathan, MRCP, Richard W. Bevan-Jones, MBBChir, Department of Psychiatry, University of Cambridge, UK; Jonathan Coles, PhD, Division of Anaesthesia, Department of Medicine, University of Cambridge, UK; Franklin Aigbirhio, DPhil, Wolfson Brain Imaging Centre and Department of Clinical Neurosciences, University of Cambridge, UK; James B. Rowe, PhD, Department of Clinical Neurosciences, University of Cambridge and Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, UK; John T. O'Brien, DM, Department of Psychiatry, University of Cambridge, UK ls514@cam.ac.uk.
Neuroinflammation, indicated by higher C-reactive protein (CRP) and [11C]PK11195 binding, is linked to late-life depression. This suggests neuroinflammation may be an early factor and a therapeutic target for dementia prevention.
Area of Science:
- Neuroscience
- Psychiatry
- Radiology
Background:
- Late-life depression is a significant risk factor for dementia.
- Neuroinflammation is increasingly recognized as a potential contributor to neurodegenerative diseases.
- Identifying biomarkers for neuroinflammation in depression is crucial for understanding dementia risk.
Purpose of the Study:
- To investigate neuroinflammation in late-life depression using positron emission tomography (PET).
- To explore the relationship between neuroinflammation markers and brain structural changes in older adults with depression.
- To assess the potential role of neuroinflammation as an etiological factor and therapeutic target in late-life depression.
Main Methods:
- Utilized [11C]PK11195 positron emission tomography (PET) to measure neuroinflammation.
- Employed multimodal 3T magnetic resonance imaging (MRI) for detailed brain structure analysis.
- Measured C-reactive protein (CRP) levels in blood samples from participants.
Main Results:
- Individuals with late-life depression exhibited significantly higher CRP levels compared to controls.
- Elevated [11C]PK11195 binding was observed in depression-associated brain regions, including the subgenual anterior cingulate cortex.
- Significant hippocampal subfield atrophy was noted in the cornu ammonis 1 and subiculum.
Conclusions:
- Neuroinflammation is a prominent feature in late-life depression.
- Findings support further investigation of neuroinflammation in late-life depression.
- Neuroinflammation may represent a viable therapeutic target for mitigating dementia risk in depressed older adults.
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