The Moderating Effect of Serum Vitamin D on the Relationship between Beta-amyloid Deposition and Neurodegeneration
- Author:
Junha PARK
1
;
Min Soo BYUN
;
Dahyun YI
;
Hyejin AHN
;
Joon Hyung JUNG
;
Nayeong KONG
;
Yoon Young CHANG
;
Gijung JUNG
;
Jun-Young LEE
;
Yu Kyeong KIM
;
Yun-Sang LEE
;
Koung Mi KANG
;
Chul-Ho SOHN
;
Dong Young LEE
;
Author Information
- Publication Type:Original Article
- From:Clinical Psychopharmacology and Neuroscience 2024;22(4):646-654
- CountryRepublic of Korea
- Language:English
-
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 (Aβ) 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 Aβ 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 Aβ deposition or HVa after controlling for age, sex, apolipoprotein E ε4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderating effect on the association between Aβ and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral Aβ-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 Aβ-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.
