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Low plasma cortisol and large hippocampal volume are associated with reduced risk of clinical progression in MCI
Author(s) -
Huijbers Willem,
Kirschbaum Clemens,
Wirth Miranka
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.044462
Subject(s) - hippocampal formation , medicine , alzheimer's disease neuroimaging initiative , biomarker , atrophy , brain size , alzheimer's disease , neuroimaging , psychology , endocrinology , hippocampus , oncology , neuroscience , disease , magnetic resonance imaging , chemistry , biochemistry , radiology
Background High cortisol concentration, a biomarker of hypothalamic‐pituitary‐adrenal (HPA) axis activation, and low hippocampal volume have been linked to increased risk for Alzheimer’s disease (AD). This longitudinal study evaluates the impact of baseline plasma cortisol levels on hippocampal atrophy and on clinical progression in patients with mild cognitive impairment (MCI). Method Participants with mild cognitive impairment (MCI, n=305) were selected from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) based on measures of plasma cortisol (at baseline) and hippocampal volume. We assessed relationships between plasma cortisol levels, hippocampal volume, and risk of progression to clinical AD over a variable study period of up to 100 months. Result Higher plasma cortisol levels were related to greater decline in hippocampal volume in MCI patients, adjusting for baseline volume (Figure 1, left). Hippocampal volume at baseline predicted progression to clinical AD, while plasma cortisol alone did not. Plasma cortisol interacted with hippocampal volume (Figure 1, right), such that MCI patients with relatively large hippocampal volumes and low plasma cortisol levels at baseline were less likely to progress to clinical AD. Conclusion This study demonstrates the involvement of plasma cortisol in hippocampal degeneration and risk of clinical progression in MCI patients. Our findings suggest that regulation of HPA axis activation may be protective against neural degradation and clinical decline in these high‐risk individuals.