Open this publication in new window or tab >>Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet, Solna, Stockholm, Sweden; Theme Inflammation and Aging. Karolinska University Hospital, Stockholm, Sweden.
Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet, Solna, Stockholm, Sweden; Ageing Epidemiology Research Unit (AGE), School of Public Health, Faculty of Medicine, Imperial College London, UK; Division of Public Health Sciences, Wake Forest University School of Medicine, North Carolina, USA; Brain and Mind Institute, Aga Khan University, Nairobi, Kenya.
Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet, Solna, Stockholm, Sweden; Theme Inflammation and Aging. Karolinska University Hospital, Stockholm, Sweden.
Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet, Solna, Stockholm, Sweden; Theme Inflammation and Aging. Karolinska University Hospital, Stockholm, Sweden; Ageing Epidemiology Research Unit (AGE), School of Public Health, Faculty of Medicine, Imperial College London, UK; Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet, Solna, Stockholm, Sweden; Theme Inflammation and Aging. Karolinska University Hospital, Stockholm, Sweden; Ageing Epidemiology Research Unit (AGE), School of Public Health, Faculty of Medicine, Imperial College London, UK; Institute of Clinical Medicine, Neurology, University of Eastern Finland, Kuopio, Finland.
Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet, Solna, Stockholm, Sweden; Division of Neurogeriatrics, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet, Stockholm, Sweden; Ageing Epidemiology Research Unit (AGE), School of Public Health, Faculty of Medicine, Imperial College London, UK.
Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet, Solna, Stockholm, Sweden; Ageing Epidemiology Research Unit (AGE), School of Public Health, Faculty of Medicine, Imperial College London, UK.
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2024 (English)In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 118, p. 499-509Article in journal (Refereed) Published
Abstract [en]
BACKGROUND: Neuroinflammation is a hallmark of the Alzheimer's disease (AD) pathogenic process. Cortisol dysregulation may increase AD risk and is related to brain atrophy. This cross-sectional study aims to examine interactions of cortisol patterns and neuroinflammation markers in their association with neuroimaging correlates.
METHOD: 134 participants were recruited from the Karolinska University Hospital memory clinic (Stockholm, Sweden). Four visual rating scales were applied to magnetic resonance imaging or computed tomography scans: medial temporal lobe atrophy (MTA), global cortical atrophy (GCA), white matter lesions (WML), and posterior atrophy. Participants provided saliva samples for assessment of diurnal cortisol patterns, and underwent lumbar punctures for cerebrospinal fluid (CSF) sampling. Three cortisol measures were used: the cortisol awakening response, total daily output, and the ratio of awakening to bedtime levels. Nineteen CSF neuroinflammation markers were categorized into five composite scores: proinflammatory cytokines, other cytokines, angiogenesis markers, vascular injury markers, and glial activation markers. Ordinal logistic regressions were conducted to assess associations between cortisol patterns, neuroinflammation scores, and visual rating scales, and interactions between cortisol patterns and neuroinflammation scores in relation to visual rating scales.
RESULT: Higher levels of angiogenesis markers were associated with more severe WML. Some evidence was found for interactions between dysregulated diurnal cortisol patterns and greater neuroinflammation-related biomarkers in relation to more severe GCA and WML. No associations were found between cortisol patterns and visual rating scales.
CONCLUSION: This study suggests an interplay between diurnal cortisol patterns and neuroinflammation in relation to brain structure. While this cross-sectional study does not provide information on causality or temporality, these findings suggest that neuroinflammation may be involved in the relationship between HPA-axis functioning and AD.
Place, publisher, year, edition, pages
Elsevier, 2024
Keywords
Alzheimer’s Disease, Cortical Atrophy, Cortisol, Cytokines, Hypothalamic-Pituitary-Adrenal Axis, Neuroimaging, Neuroinflammation, Visual Rating Scales, White Matter Lesions
National Category
Neurosciences
Identifiers
urn:nbn:se:hj:diva-63933 (URN)10.1016/j.bbi.2024.03.024 (DOI)001216219600001 ()38503394 (PubMedID)2-s2.0-85188779839 (Scopus ID)
2024-04-032024-04-032024-05-21Bibliographically approved