The Moderating Effect of Serum Vitamin D on the Relationship between Beta-amyloid Deposition and Neurodegeneration
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Objective: Previous studies have reported that vitamin D deficiency increased the risk of Alzheimer’s disease (AD) dementia in older adults. However, little is known about how vitamin D is involved in the pathophysiology of AD. Thus, this study aimed to examine the association and interaction of serum vitamin D levels with in vivo AD pathologies including cerebral beta-amyloid (A) deposition and neurodegeneration in nondemented older adults. Methods: 428 Nondemented older adults were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease, a prospective cohort that began in 2014. All participants underwent comprehensive clinical assessments, measurement of serum 25-hydroxyvitamin D (25[OH]D), and multimodal brain imaging including Pittsburgh compound B (PiB) positron emission tomography and magnetic resonance imaging. Global PiB deposition was measured for the A biomarker. Intracranial volume-adjusted hippocampal volume (HVa) was used as a neurodegeneration biomarker. Results: Overall, serum 25(OH)D level was not associated with either A deposition or HVa after controlling for age, sex, apolipoprotein E 4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderating effect on the association between A and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral A-associated hippocampal volume loss (B = 34.612, p = 0.008). Conclusion: Our findings indicate that lower serum vitamin D levels may contribute to AD by exacerbating A-associated neurodegeneration in nondemented older adults. Further studies to explore the potential therapeutic effect of vitamin D supplementation on the progression of AD pathology will be necessary.
Abstract
Objective: Previous studies have reported that vitamin D deficiency increased the risk of Alzheimer’s disease (AD) dementia in older adults. However, little is known about how vitamin D is involved in the pathophysiology of AD. Thus, this study aimed to examine the association and interaction of serum vitamin D levels with in vivo AD pathologies including cerebral beta-amyloid (A) deposition and neurodegeneration in nondemented older adults. Methods: 428 Nondemented older adults were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease, a prospective cohort that began in 2014. All participants underwent comprehensive clinical assessments, measurement of serum 25-hydroxyvitamin D (25[OH]D), and multimodal brain imaging including Pittsburgh compound B (PiB) positron emission tomography and magnetic resonance imaging. Global PiB deposition was measured for the A biomarker. Intracranial volume-adjusted hippocampal volume (HVa) was used as a neurodegeneration biomarker. Results: Overall, serum 25(OH)D level was not associated with either A deposition or HVa after controlling for age, sex, apolipoprotein E 4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderating effect on the association between A and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral A-associated hippocampal volume loss (B = 34.612, p = 0.008). Conclusion: Our findings indicate that lower serum vitamin D levels may contribute to AD by exacerbating A-associated neurodegeneration in nondemented older adults. Further studies to explore the potential therapeutic effect of vitamin D supplementation on the progression of AD pathology will be necessary.
참고문헌 (49)
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