Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the influence of immobilization-induced hypercalcemia on bone metabolism in Parkinson's disease (PD), we measured serum biochemical indexes and bone mineral density (BMD) in the second metacarpals of 142 elderly PD patients and 99 age-matched healthy controls. Serum concentrations of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-[OH](2)D), ionized calcium, intact parathyroid hormone (PTH), and intact bone Gla protein (BGP) were measured. Urinary deoxypyridinoline (D-Pyr) was also measured. Increased serum calcium levels (mean, 1.27 mmol/L) were observed in PD patients, and the levels correlated negatively with the Unified Parkinson's Disease Rating Scale III (UPDRS III), indicating the presence of immobilization-induced bone resorption with resultant hypercalcemia. Decreased serum concentrations of 1,25-[OH](2)D (mean, 88.7 pmol/L) and 25-OHD (mean, 29.7 nmol/L) were noted. Serum PTH was decreased (mean, 25.2 ng/L). Serum BGP was decreased while urinary D-Pyr concentration elevated. A negative correlation was observed between 1,25-[OH](2)D levels and serum calcium or UPDRS III (P < 0.0001). In disabled PD patients, immobilization-induced hypercalcemia may inhibit secretion of PTH, which in turn suppresses 1,25-[OH](2)D production. 25-OHD insufficiency may also contribute to decreased 1,25-[OH](2)D. These abnormalities may be corrected by the suppression of bone resorption with bisphoshonate, and supplementations of calcium and vitamin D should be avoided in these patients.
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PMID:Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients. 3065 27

Parkinson's disease is associated with an increased risk of falls. The risk is greatest in patients with advanced disease. Because Parkinson's disease usually occurs late in life, the risk factors related to the neurological impairments add to those associated with aging. The incidence of fractures is high in patients with Parkinson's disease, with femoral neck fractures in older women being particularly common. Risk factors for fractures include a low body mass index, limited exposure to sunlight, an inadequate vitamin D intake with low 25-OH vitamin D levels, and bone loss. Several studies found decreased bone mineral density values at the femoral neck and lumbar spine in patients with Parkinson's disease. Although this decrease is ascribable in part to factors unrelated with Parkinson's disease, such as older age and female gender, Parkinson's disease itself also plays a role, most notably in patients with severe neurological impairments (Hoehn and Yahr stages III and IV).
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PMID:Parkinson's disease and osteoporosis. 1637 2

The presence of vitamin D receptors (VDRs) in the brain suggest that vitamin D had functions in this organ and accumulating data have provide evidence that this is indeed the case. Recently, it has been recognized that vitamin D behaves as a neuroactive compound (neurosteroid) largely implicated in the control of brain homeostasis. Likewise, the neuroprotective effects of vitamin D, achieved by its action levels of nerve growth factors in the treatment of neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD). Recent studies on VDR gene knockout mice revealed that VDR also regulates behavioural characterization and differentiation of skeletal muscle. Thus, vitamin D appears to regulate development and homeostasis of the nervous system and skeletal muscle.
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PMID:[Effect of vitamin D on the nervous system and the skeletal muscle]. 1681 79

There is some evidence suggesting that Parkinson's disease (PD) patients exhibit lower body weight when compared to age-matched healthy subjects. Low body mass index (BMI) is correlated with low bone mineral density, both of which are major risk factors for hip fractures. Possible determinants of weight loss in PD patients include hyposmia, impaired hand-mouth coordination, difficulty chewing, dysphagia, intestinal hypomotility, depression, decreased reward processing of dopaminergic mesolimbic regions, nausea, and anorexia as the side effects of medication, and increased energy requirements due to muscular rigidity and involuntary movements. It is unclear whether PD patients in general, or only a subgroup of those affected, definitely show lower BMI in the advanced stages of the disease. We therefore recommend that the body weight of PD patients be monitored monthly as the disease progresses, and that a patient's nutrition should be supplemented with sufficient amounts of vitamin D and calcium to reduce the risk of hip fractures and strengthen bone density. Because meal times may coincide with unpredictable off periods associated with akinesia and impaired hand-mouth coordination, PD patients also need flexible food schedules that accommodate the associated symptoms of this disease.
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PMID:Body weight in patients with Parkinson's disease. 1751 85

Parkinson's disease (PD), a common disease of the elderly, is a movement disorder characterized by tremor, akinesia, and loss of postural reflexes, leading to immobility and frequent falls. It results from selective loss (death) of dopaminergic neurons in the substantia nigra region of the brain, largely developed prior to clinical diagnosis, and continuous after diagnosis, despite use of current therapeutic modalities. In PD in the United States the cause and mechanism of continued neuron cell death in the substantia nigra is currently unknown. We hypothesize, based upon several lines of evidence, that documented chronically inadequate vitamin D intake in the United States, particularly in the northern states and particularly in the elderly, is a significant factor in the pathogenesis of PD. This hypothesis implies that dietary aid for prevention and therapy for PD is possible.
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PMID:Vitamin D and Parkinson's disease--a hypothesis. 1723 Apr 73

Falls occur commonly in older persons and are the seventh leading cause of death. Falls are associated with functional deterioration and "fear of falling". Falls can be due to extrinsic factors such as poor lighting, throw rugs and other environmental hazards. Intrinsic causes of falls include physiological changes associated with aging, orthostatic hypotension, many medications, delirium, anemia, diabetes mellitus, Parkinson's disease, depression, cognitive impairment, syncope, partial complex seizures and vitamin D deficiency. Management of falls requires a multidisciplinary approach with a home assessment and modification where appropriate, a careful geriatric assessment, exercise programs focusing on balance, resistance and endurance exercise and adequate vitamin D replacement. All fallers should be assessed and treated for osteoporosis. The complexities of the causes and management of falls, make persons with frequent falls an ideal person to be referred for a geriatric consult.
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PMID:Falls--where do we stand? 1741 Aug 28

It has been known for more than 20 years that vitamin D exerts marked effects on immune and neural cells. These non-classical actions of vitamin D have recently gained a renewed attention since it has been shown that diminished levels of vitamin D induce immune-mediated symptoms in animal models of autoimmune diseases and is a risk factor for various brain diseases. For example, it has been demonstrated that vitamin D (i) modulates the production of several neurotrophins, (ii) up-regulates Interleukin-4 and (iii) inhibits the differentiation and survival of dendritic cells, resulting in impaired allo-reactive T cell activation. Not surprisingly, vitamin D has been found to be a strong candidate risk-modifying factor for Multiple Sclerosis (MS), the most prevalent neurological and inflammatory disease in the young adult population. Vitamin D is a seco-steroid hormone, produced photochemically in the animal epidermis. The action of ultraviolet light (UVB) on 7-dehydrocholesterol results in the production of pre-vitamin D which, after thermo-conversion and two separate hydroxylations, gives rise to the active 1,25-dihydroxyvitamin D. Vitamin D acts through two types of receptors: (i) the vitamin D receptor (VDR), a member of the steroid/thyroid hormone superfamily of transcription factors, and (ii) the MARRS (membrane associated, rapid response steroid binding) receptor, also known as Erp57/Grp58. In this article, we review some of the mechanisms that may underlie the role of vitamin D in various brain diseases. We then assess how vitamin D imbalance may lay the foundation for a range of adult disorders, including brain pathologies (Parkinson's disease, epilepsy, depression) and immune-mediated disorders (rheumatoid arthritis, type I diabetes mellitus, systemic lupus erythematosus or inflammatory bowel diseases). Multidisciplinary scientific collaborations are now required to fully appreciate the complex role of vitamin D in mammal metabolism.
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PMID:Vitamin D, a neuro-immunomodulator: implications for neurodegenerative and autoimmune diseases. 1954 51

This is a mini-review of vitamin D(3), its active metabolites and their functioning in the central nervous system (CNS), especially in relation to nervous system pathologies and aging. The vitamin D(3) endocrine system consists of 3 active calcipherol hormones: calcidiol (25OHD(3)), 1alpha-calcitriol (1alpha,25(OH)2D(3)) and 24-calcitriol (24,25(OH)2D(3)). The impact of the calcipherol hormone system on aging, health and disease is discussed. Low serum calcidiol concentrations are associated with an increased risk of several chronic diseases including osteoporosis, cancer, diabetes, autoimmune disorders, hypertension, atherosclerosis and muscle weakness all of which can be considered aging-related diseases. The relationship of many of these diseases and aging-related changes in physiology show a U-shaped response curve to serum calcidiol concentrations. Clinical data suggest that vitamin D(3) insufficiency is associated with an increased risk of several CNS diseases, including multiple sclerosis, Alzheimer's and Parkinson's disease, seasonal affective disorder and schizophrenia. In line with this, recent animal and human studies suggest that vitamin D insufficiency is associated with abnormal development and functioning of the CNS. Overall, imbalances in the calcipherol system appear to cause abnormal function, including premature aging, of the CNS.
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PMID:Vitamin D, nervous system and aging. 1966 Aug 71

Epidemiological and experimental evidence suggest that vitamin D deficiency is a risk factor for multiple sclerosis and other autoimmune diseases. The activated form of vitamin D exerts several immunomodulating properties in vitro and in vivo, that could contribute to explain the association with multiple sclerosis. Hypovitaminosis D is also associated with several other neurological diseases that is less likely mediated by dysregulated immune responses, including Parkinson's disease and Alzheimer's disease, schizophrenia and affective disorders, suggesting a more diverse role for vitamin D in the maintenance of brain health. Accordingly, both the vitamin D receptor and the enzymes necessary to synthesize bioactive 1,25-dihydroxyvitamin D are expressed in the brain, and hypovitaminosis D is associated with abnormal development and function of the brain. We here review current knowledge on the intrathecal vitamin D homeostasis in heath and disease, highlighting the need to assess vitamin D in the intrathecal compartment.
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PMID:Assessing vitamin D in the central nervous system. 2058 43

Pathological hallmarks of Parkinson's disease are destruction of dopaminergic neurons in the basal ganglia, especially the substantia nigra, and the presence of Lewy bodies within nerve cells. Environmental toxins are associated with the disease and, in a minority of cases, genetic factors have been identified. Inflammation-with activation of phagocytic microglia, release of cytokines, invasion by T cells, and complement activation-plays a role in damaging these neurons. Excessive production of reactive oxygen species, mitochondrial dysfunction leading to apoptosis, accumulation and oligomerization of the protein alpha-synuclein, and defective protein disposal by the ubiquitin proteasome system are involved in the complex web of events mediating nigral cell demise. Two agents of current interest, coenzyme Q10 and creatine, may be disease modifying, and large studies are in progress. Related mechanisms of other substances, including omega-3 fatty acids and vitamin D, are included in this review. The association with serum cholesterol levels and the effects of statin drugs are uncertain but important.
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PMID:Parkinson's disease: mitochondrial molecular pathology, inflammation, statins, and therapeutic neuroprotective nutrition. 2070 43


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