An algorithmic approach to understand trace elemental homeostasis in serum samples of Parkinson disease

Pande, Madhura; Nagabhushan, P.; Hegde, Muralidhar L.; Rao, T.S. Sathyanarayana; Rao, K. S.

doi:10.1016/j.compbiomed.2004.04.003

Cited by 6 publications

(1 citation statement)

References 14 publications

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“…Although several reports are available on individual metal level changes/distribution, no studies have successfully correlated the inter-elemental relationships. Our limited previous studies provided new information on the metal-homeostasis pattern in the brain and serum samples of AD/PD patients [ 1 , 173 ]. Due to the tight regulation of charge balance in a cell and across the membrane, the effect of changes in the level of a particular metal is not restricted to that metal alone, but instead, it would impact many other metals in that particular organ and, eventually, lead to metal dyshomeostasis and cellular dysfunction.…”

Section: Revisiting Metal Toxicity Diseasesmentioning

confidence: 99%

New Perspectives on Oxidized Genome Damage and Repair Inhibition by Pro-Oxidant Metals in Neurological Diseases

et al. 2014

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The primary cause(s) of neuronal death in most cases of neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease, are still unknown. However, the association of certain etiological factors, e.g., oxidative stress, protein misfolding/aggregation, redox metal accumulation and various types of damage to the genome, to pathological changes in the affected brain region(s) have been consistently observed. While redox metal toxicity received major attention in the last decade, its potential as a therapeutic target is still at a cross-roads, mostly because of the lack of mechanistic understanding of metal dyshomeostasis in affected neurons. Furthermore, previous studies have established the role of metals in causing genome damage, both directly and via the generation of reactive oxygen species (ROS), but little was known about their impact on genome repair. Our recent studies demonstrated that excess levels of iron and copper observed in neurodegenerative disease-affected brain neurons could not only induce genome damage in neurons, but also affect their repair by oxidatively inhibiting NEIL DNA glycosylases, which initiate the repair of oxidized DNA bases. The inhibitory effect was reversed by a combination of metal chelators and reducing agents, which underscore the need for elucidating the molecular basis for the neuronal toxicity of metals in order to develop effective therapeutic approaches. In this review, we have focused on the oxidative genome damage repair pathway as a potential target for reducing pro-oxidant metal toxicity in neurological diseases.

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Section: Revisiting Metal Toxicity Diseasesmentioning

confidence: 99%

New Perspectives on Oxidized Genome Damage and Repair Inhibition by Pro-Oxidant Metals in Neurological Diseases

et al. 2014

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Lower calcium levels in hair of Parkinson’s disease patients are associated with presence of sleeping disturbances

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Bezerra

Rocha

et al. 2021

Nutritional Neuroscience

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Elevated circulating magnesium levels in patients with Parkinson’s disease: a meta-analysis

Jin

Liu

Zhang

et al. 2018

NDT

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BackgroundThe association between circulating magnesium (Mg) and Parkinson’s disease (PD) remains ambiguous and controversial. Thus, a meta-analysis was conducted to evaluate the circulating Mg levels in PD patients and to clarify whether high circulating Mg levels should be considered as a potential risk factor for PD.MethodsIn this study, 17 case–control published studies were selected in our meta-analysis by searching the electronic databases of Web of Science, PubMed, and China National Knowledge Infrastructure (CNKI) before June 1, 2018. Overall, 848 PD cases and 784 healthy controls (HC), 1,023 PD cases and 911 HC, and 180 PD cases and 144 HC met the inclusion criteria for this study Mg levels in serum, peripheral blood, and cerebrospinal fluid (CSF), respectively. Standardized mean difference (SMD) in random-effects model and 95% CI were used to assess the correlation strength through the comparison of the two groups.ResultsMeta-analysis showed that the serum Mg levels in PD cases were significantly higher than those in HC individuals (SMD =1.09, 95% CI =0.52, 1.66). Furthermore, this result was further confirmed by the combined analysis of serum and whole blood studies together (SMD =0.64, 95% CI =0.10, 1.19). In addition, the higher CSF Mg levels in patients of PD were observed in comparison with normal range (SMD =0.55, 95% CI =0.21, 0.88). However, this data did not further discuss and analyze because of the smaller sample size of CSF studies.ConclusionOur findings supported the notion that the increase of circulating Mg levels appears in the patients with PD.

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An algorithmic approach to understand trace elemental homeostasis in serum samples of Parkinson disease

Cited by 6 publications

References 14 publications

New Perspectives on Oxidized Genome Damage and Repair Inhibition by Pro-Oxidant Metals in Neurological Diseases

New Perspectives on Oxidized Genome Damage and Repair Inhibition by Pro-Oxidant Metals in Neurological Diseases

Lower calcium levels in hair of Parkinson’s disease patients are associated with presence of sleeping disturbances

Elevated circulating magnesium levels in patients with Parkinson’s disease: a meta-analysis

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An algorithmic approach to understand trace elemental homeostasis in serum samples of Parkinson disease

Cited by 6 publications

References 14 publications

New Perspectives on Oxidized Genome Damage and Repair Inhibition by Pro-Oxidant Metals in Neurological Diseases

New Perspectives on Oxidized Genome Damage and Repair Inhibition by Pro-Oxidant Metals in Neurological Diseases

Lower calcium levels in hair of Parkinson’s disease patients are associated with presence of sleeping disturbances

Elevated circulating magnesium levels in patients with Parkinson&rsquo;s disease: a meta-analysis

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Elevated circulating magnesium levels in patients with Parkinson’s disease: a meta-analysis