PARATHYROID HORMONE, VITAMIN D, AND COGNITIVE DECLINE IN OLDER PEOPLE WITH A HISTORY OF VASCULAR DISEASES
M.P. Björkman, K.H. Pitkala, T.E. Strandberg, R.S. Tilvis
J Aging Res Clin Practice 2013;2(1):121-125
Introduction: Cross-sectional and prospective follow-up studies have suggested serum 25-hydroxyvitamin D (25-OHD) to associate with cognitive decline. However, other regulators of calcium homeostasis, such as parathyroid hormone (PTH), may confound this association. In this prospective three-year follow-up study the predictive value of both 25-OHD and PTH for cognitive decline were investigated. Methods: Older community-dwelling people (N=400, age=80±5 years) with a history of vascular diseases were included. In addition to thorough clinical examination cognition was assessed by Consortium to Establish a Registry for Alzheimer Disease neuropsychological assessment battery total score (CERAD) at baseline and after three-year follow-up. Baseline serum 25-OHD, PTH, total calcium, creatinine and apolipoprotein E4 genotype were determined. Results: The mean baseline MMSE score was 26±3 and that of total CERAD score 69±12. A weak inverse association was observed between baseline PTH levels and CERAD total scores (r= -0.120, p=0.023). The highest baseline PTH quartile (≥83.1 ng/l) compared with lower quartiles was associated with 2.4-fold risk (95%CIs=1.05-5.35) for at least 10-point decline in CERAD total score within three years. The risk remained significant after controlling for age, gender, education, apolipoprotein E4, baseline CERAD score, body mass index, creatinine, total calcium, and 25-hydrovitamin D. No significant associations were found between baseline 25-OHD and cognition in cross-sectional or longitudinal analyses. Conclusion: High baseline levels of PTH are associated independently of baseline vitamin D status with clinically significant cognitive decline in older community-dwelling people with a history of vascular diseases. Further studies are warranted to address the role of PTH and its regulators in the etiology of cognitive impairment.