![]() Cognitive impairment has also been observed in this parathyroid condition followed by postoperative improvement. Failing kidneys may cause secondary hyperparathyroidism and therefore the condition is frequently occurring in chronic kidney disease. Secondary hyperparathyroidism is determined by high PTH levels, normal to low calcium levels and concurrent decrease in vitamin D levels. Although not supported by all studies, there is evidence from surgical studies that parathyroidectomy, which if successful leads to normalization of PTH and calcium levels, is associated with significant improvement in cognitive function or even reversibility of cognitive deficits. Patients with primary hyperparathyroidism (high PTH and calcium levels), the most common parathyroid disease, often report cognitive complaints and observational studies have described poorer cognitive function in those patients compared to control groups including impaired performance in memory and attention tasks. Hyperparathyroidism, characterized by elevated/high PTH levels, has been associated with many chronic conditions including impaired cognitive function and dementia. PTH also promotes the conversion of vitamin D to its active form (1,25-dihydroxyvitamin D), which an emerging body of evidence suggests may be neuroprotective. Elevated PTH levels are associated with reduced regional cerebral blood flow, whereas PTH-related protein (PTHrP) inhibited calcium channel activity via the PTH/PTHrP receptor may contribute to maintaining normal neuronal function (for example by increasing resistance to excitotoxic injury). PTH regulates circulating and intracellular calcium levels, and may induce apoptosis due to calcium overloading. Parathyroid hormone (PTH) is of interest in relation to cognitive function and dementia as it crosses the blood brain barrier and PTH receptors are found throughout the human brain. In the absence of disease modifying or curative treatments, the identification of potentially modifiable risk factors for Alzheimer’s disease and other dementia subtypes is particularly important. DJL is funded by the Alzheimer’s Association, the Rosetrees Trust, the Mary Kinross Charitable Trust, the James Tudor Foundation, the Halpin Trust, and the Norman Family Charitable Trust.Ĭompeting interests: The authors have declared that no competing interests exist. The views expressed in this publication are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedĭata Availability: All relevant data are within the paper and its Supporting Information files.įunding: This research has been supported by the National Institute for Health Research (NIHR) South West Peninsula Collaboration for Leadership in Applied Health Research and Care (PenCLAHRC). ![]() Received: FebruAccepted: ApPublished: May 26, 2015Ĭopyright: © 2015 Lourida et al. Quinn, University of Glasgow, UNITED KINGDOM PLoS ONE 10(5):Īcademic Editor: Terence J. (2015) Parathyroid Hormone, Cognitive Function and Dementia: A Systematic Review. Likewise, if you’re not eating enough food sources of calcium (spinach, dairy, soybeans, among others), low calcium levels could trigger an overproduction of PTH.Citation: Lourida I, Thompson-Coon J, Dickens CM, Soni M, Kuźma E, Kos K, et al. If you don’t get enough vitamin D in your diet or you don’t get enough sun exposure (your body converts sunlight into vitamin D), your calcium levels can drop dramatically. Vitamin D helps balance your calcium levels. Two of the main triggers of low calcium are vitamin D deficiency and dietary calcium deficiency. As a result, the parathyroid glands work harder to try to boost your calcium. Secondary hyperparathyroidism occurs when you have some other health condition that reduces your calcium levels. Other causes of primary hyperparathyroidism include hyperplasia or the enlargement of two more glands. A cancerous or noncancerous growth on one of these glands may cause it to function abnormally. With primary hyperparathyroidism, there is a problem with the parathyroid glands. There appear to be two main causes of osteitis fibrosa cystica: primary hyperparathyroidism and secondary hyperparathyroidism. Some bones may have weak areas with little or no calcium. In some cases, PTH isn’t enough to overcome low calcium levels. If calcium levels drop, the glands increase their PTH production.īones can respond to PTH differently. When calcium levels get too high, the parathyroid glands make less PTH. They produce PTH, which helps your body maintain healthy levels of calcium and phosphorous in your bloodstream and in tissue throughout your body. You have four tiny parathyroid glands in your neck.
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