17 January 2014
A new study exploring vitamin D levels in patients with Parkinson’s disease (PD) opens up the possibility of a new avenue of early intervention that may delay or prevent the onset of cognitive impairment and depression. The findings are published in the Journal of Parkinson’s Disease.
Investigators conducted a cross-sectional analysis of 286 patients with PD and found that higher plasma vitamin D levels were associated with lower symptom severity, better cognition, and less depression in the entire group, but the relationships were even stronger in those who were not demented.
“About 30% of persons with PD suffer from cognitive impairment and dementia, and dementia is associated with nursing home placement and shortened life expectancy,” says Amie L. Peterson, MD, of the Oregon Health and Sciences University. “We know mild cognitive impairment may predict the future development of dementia. Intervening in the development of dementia has the potential to improve morbidity and mortality in persons with PD.”
In this analysis, which was an add-on study to an ongoing longitudinal study of neuropsychiatric function in people with PD, patients were given a battery of tests measuring global cognitive function, verbal memory, semantic verbal fluency, executive function, and depression. On the same day, serum 25-hydroxyvitamin D levels were measured. Of the 286 subjects, 61 were considered to be demented by a consensus panel based on the Diagnostic and Statistical Manual of the American Psychiatric Association (4th edition) and 225 were not demented.
For the entire group, significant negative associations were found between vitamin D levels and disease severity, as measured both by the Hoehn and Yahr Scale and the United Parkinson’s Disease Rating Scale motor section. Mean vitamin D3 levels were higher in those who were not demented, although the differences did not reach statistical significance.
Investigators found that for the entire group, higher levels of serum vitamin D3 were associated with greater fluency for naming vegetables and animals and immediate and delayed recall on a verbal learning test. When the group was divided into those who were demented or not, significant findings with vitamin D were found for fluency and verbal learning only for those who were not demented. “The fact that the relationship between vitamin D concentration and cognitive performance seemed more robust in the non-demented subset suggests that earlier intervention before dementia is present may be more effective,” says Dr. Peterson.
A significant negative association was also found for vitamin D levels and depression, as measured by the Geriatric Depression Scale, for both the entire group and those who were not demented. No significant relationship was found for those who were demented.
The authors point out that a cross-sectional study cannot determine causation: for instance, does low vitamin D affect cognitive performance, or are persons with more advanced PD and worse cognition less ambulatory, get less sun exposure, and subsequently have lower vitamin D? The study also did not consider if patients were taking vitamin D supplements.
Vitamin D’s role in health has been a subject of considerable scrutiny in recent years. Low levels increase the risk of type 2 diabetes mellitus, multiple sclerosis, hypertension, cancer, and infections. Vitamin D receptors and its final converting enzyme have been found in human brain tissue, including the hippocampus, which plays a significant role in memory and learning.
PD is the second most common neurodegenerative disorder in the United States, affecting approximately one million Americans and five million people worldwide. Its prevalence is projected to double by 2030. The most obvious symptoms are movement-related, such as involuntary shaking and muscle stiffness. Non-motor symptoms, such as worsening depression, anxiety, and sleep disturbances, can appear prior to the onset of motor symptoms.
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NOTES FOR EDITORS
“Memory, Mood, and Vitamin D in Persons with Parkinson’s Disease,” by Amie L. Peterson, Charles Murchison, Cyrus Zabetian, James Leverenz, G. Stennis Watson, Thomas Montine, Natasha Carney, Gene L. Bowman, Karen Edward, and Joseph F. Quinn. Journal of Parkinson’s Disease, Volume 3/Issue 4, DOI: 10.3233/JPD-130206. Published by IOS Press.
Full text of the article is available to credentialed journalists upon request. Contact Daphne Watrin, IOS Press, +31 20 688 3355, d.watrin@iospress.nl to obtain a copy or for additional information.
ABOUT THE JOURNAL OF PARKINSON’S DISEASE (JPD)
Launched in June 2011 the Journal of Parkinson’s Disease is dedicated to providing an open forum for original research in basic science, translational research and clinical medicine that will expedite our fundamental understanding and improve treatment of Parkinson’s disease. The journal is international and multidisciplinary and aims to promote progress in the epidemiology, etiology, genetics, molecular correlates, pathogenesis, pharmacology, psychology, diagnosis and treatment of Parkinson’s disease. It publishes research reports, reviews, short communications, and letters-to-the- editor and offers very rapid publication and an affordable open access option.
ABOUT IOS PRESS
Commencing its publishing activities in 1987, IOS Press (www.iospress.nl) serves the information needs of scientific and medical communities worldwide. IOS Press now (co-)publishes over 100 international journals and about 130 book titles each year on subjects ranging from computer sciences and mathematics to medicine and the natural sciences.
IOS Press continues its rapid growth, embracing new technologies for the timely dissemination of information. All journals are available electronically and an e-book platform was launched in 2005.
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