Iron as a risk factor in neurological diseases

2008 ◽  
Vol 182 (1-3) ◽  
pp. 31-44 ◽  
Author(s):  
Jolanta Galazka-Friedman
Keyword(s):  
Risk Factor ◽  
Neurological Diseases

scholarly journals Impaired regulation of KCC2 phosphorylation leads to neuronal network dysfunction and neurodevelopmental pathology

2019 ◽  
Vol 12 (603) ◽  
pp. eaay0300 ◽  
Author(s):  
Lucie I. Pisella ◽  
Jean-Luc Gaiarsa ◽  
Diabé Diabira ◽  
Jinwei Zhang ◽  
Ilgam Khalilov ◽  
...  
Keyword(s):  
Risk Factor ◽  
Social Behavior ◽  
Neurological Diseases ◽  
Ultrasonic Vocalizations ◽  
Network Activity ◽  
Gabaergic Inhibition ◽  
Developmental Sequence ◽  
Normal Cells ◽  
Neurological Pathology

KCC2 is a vital neuronal K+/Cl− cotransporter that is implicated in the etiology of numerous neurological diseases. In normal cells, KCC2 undergoes developmental dephosphorylation at Thr906 and Thr1007. We engineered mice with heterozygous phosphomimetic mutations T906E and T1007E (KCC2E/+) to prevent the normal developmental dephosphorylation of these sites. Immature (postnatal day 15) but not juvenile (postnatal day 30) KCC2E/+ mice exhibited altered GABAergic inhibition, an increased glutamate/GABA synaptic ratio, and greater susceptibility to seizure. KCC2E/+ mice also had abnormal ultrasonic vocalizations at postnatal days 10 to 12 and impaired social behavior at postnatal day 60. Postnatal bumetanide treatment restored network activity by postnatal day 15 but failed to restore social behavior by postnatal day 60. Our data indicate that posttranslational KCC2 regulation controls the GABAergic developmental sequence in vivo, indicating that deregulation of KCC2 could be a risk factor for the emergence of neurological pathology.

Organic Metal Species as Risk Factor for Neurological Diseases

2016 ◽  
pp. 97-116
Author(s):  
Sören Meyer ◽  
Till Weber ◽  
Robert Haferkorn-Starke ◽  
Tanja Schwerdtle ◽  
Julia Bornhorst
Keyword(s):  
Risk Factor ◽  
Neurological Diseases ◽  
Metal Species ◽  
Organic Metal

scholarly journals CHRONIC NEUROLOGICAL DISEASE AS AN INDEPENDENT RISK FACTOR FOR DEATH IN SEVERE COVID-19 CASES

2021 ◽  
Vol 20 (2) ◽  
pp. 224-227
Author(s):  
Elena Caires Silveira ◽  
Keyword(s):  
Risk Factors ◽  
Regression Analysis ◽  
Risk Factor ◽  
Poisson Regression ◽  
Neurological Disease ◽  
Independent Risk Factor ◽  
Neurological Diseases ◽  
P Value ◽  
Poisson Regression Analysis ◽  
Multisystemic Disease

COVID-19 is a multisystemic disease with a wild severity range, being some chronic diseases risk factors for unfavorable evolution. It has been suggested are chronic neurological diseases are associated to higher mortality in COVID-19 patients; such association however, has not been described enough. In this context, this study seeks to evaluate whether the presence of previous chronic neurological disease is a factor associated with higher mortality in hospitalized severe cases of COVID-19. For this, the association between those variables was investigated in 87,871 patients through univariate (risk ratio and χ2 test) and multivariate (Poisson regression) analysis. It was found that the mortality rate for patients presenting chronic neurological disease was 23% higher (),this being an independent and statistically significant association (RR = 1.23, 95% CI = 1.2-1.3; p-value < 0.001). Therefore, more studies are needed to better characterize this association.

scholarly journals Implication of Hyperhomocysteinemia in Blood Retinal Barrier (BRB) Dysfunction

Biomolecules ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1119 ◽  
Author(s):  
Amany Tawfik ◽  
Yara A. Samra ◽  
Nehal M. Elsherbiny ◽  
Mohamed Al-Shabrawey
Keyword(s):  
Oxidative Stress ◽  
Risk Factor ◽  
Vision Loss ◽  
Neurological Diseases ◽  
Brain Inflammation ◽  
Age Related Macular Degeneration ◽  
Matrix Remodeling ◽  
Blood Retinal Barrier ◽  
Age Related

Elevated plasma homocysteine (Hcy) level, known as hyperhomocysteinemia (HHcy) has been linked to different systemic and neurological diseases, well-known as a risk factor for systemic atherosclerosis and cardiovascular disease (CVD) and has been identified as a risk factor for several ocular disorders, such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). Different mechanisms have been proposed to explain HHcy-induced visual dysfunction, including oxidative stress, upregulation of inflammatory mediators, retinal ganglion cell apoptosis, and extracellular matrix remodeling. Our previous studies using in vivo and in vitro models of HHcy have demonstrated that Hcy impairs the function of both inner and outer blood retinal barrier (BRB). Dysfunction of BRB is a hallmark of vision loss in DR and AMD. Our findings highlighted oxidative stress, ER stress, inflammation, and epigenetic modifications as possible mechanisms of HHcy-induced BRB dysfunction. In addition, we recently reported HHcy-induced brain inflammation as a mechanism of blood–brain barrier (BBB) dysfunction and pathogenesis of Alzheimer’s disease (AD). Moreover, we are currently investigating the activation of glutamate receptor N-methyl-d-aspartate receptor (NMDAR) as the molecular mechanism for HHcy-induced BRB dysfunction. This review focuses on the studied effects of HHcy on BRB and the controversial role of HHcy in the pathogenesis of aging neurological diseases such as DR, AMD, and AD. We also highlight the possible mechanisms for such deleterious effects of HHcy.

scholarly journals Assessing Causal Links Between Cytokines and Human Phenotypes: Mendelian-Randomization Study

2021 ◽  
Author(s):  
Shucheng Si ◽  
Fuzhong Xue ◽  
Kai Zhang
Keyword(s):  
Risk Factor ◽  
Bayesian Model Averaging ◽  
Mendelian Randomization ◽  
Neurological Diseases ◽  
Model Averaging ◽  
Complex Diseases ◽  
Causal Effects ◽  
Inverse Variance ◽  
Human Complex

Abstract Background: Cytokines have been implicated in the initiation of human complex diseases, and the causality between cytokines and human phenotypes has not been systematically explored.Methods: Bidirectional mendelian randomization (MR) and multivariate mendelian randomization (MVMR) with Bayesian model averaging (MR-BMA) were performed to explore the causality of 41 cytokines and 83 human phenotypes.Results: Inverse variance weighted (IVW) MR showed that MIG, SCGFb, SCF, and MIF had causal effects on ovarian, colon, breast cancer, and their subtypes. Similarly, MCP1, TRAIL, and SCGFb had causal effects on heart failure (HF), stroke and its subtypes, coronary heart disease (CHD), and myocardial infarction (MI). About neurological diseases: MIP1b had positively causal effects on Alzheimer's disease (AD) and Parkinson's disease (PD), and MIG increased the risk of AD. MR-BMA showed that MIP1b was the top priority risk factor for AD and PD; MCP1 was the top risk factor for HF, stroke, and gout; SCF was the top risk factor for ovarian cancer; PDGFbb and SCGFb were the top risk factor for ischemic stroke (IS) (cardioembolic) and type 1 diabetes, respectively. The results of bidirectional MR showed endocrine diseases and autoimmune diseases influenced the circulating levels of cytokines.Conclusions: Our findings showed that cytokines have extensive causal effects on human complex diseases. Chemokines (MCP1, MIP1b) and growth factors (PDGFbb, SCGFb, SCF) could be recommended as valuable biomarkers of chronic diseases.

scholarly journals Iatrogenic Iron Promotes Neurodegeneration and Activates Self-Protection of Neural Cells against Exogenous Iron Attacks

Function ◽  
2021 ◽  
Vol 2 (2) ◽  
Author(s):  
Maosheng Xia ◽  
Shanshan Liang ◽  
Shuai Li ◽  
Ming Ji ◽  
Beina Chen ◽  
...  
Keyword(s):  
Risk Factor ◽  
Glial Cells ◽  
Neurological Diseases ◽  
Common Element ◽  
Neural Cells ◽  
Divalent Metal Transporter 1 ◽  
Divalent Metal Transporter ◽  
Excess Iron ◽  
Metal Implants

Abstract Metal implants are used worldwide, with millions of nails, plates, and fixtures grafted during orthopedic surgeries. Iron is the most common element of these metal implants. As time passes, implants can be corroded and iron can be released. Ionized iron permeates the surrounding tissues and enters circulation; importantly, iron ions pass through the blood–brain barrier. Can iron from implants represent a risk factor for neurological diseases? This remains an unanswered question. In this study, we discovered that patients with metal implants delivered through orthopedic surgeries have higher incidence of Parkinson’s disease or ischemic stroke compared to patients who underwent similar surgeries but did not have implants. Concentration of serum iron and ferritin was increased in subjects with metal implants. In experiments in vivo, we found that injection of iron dextran selectively decreased the presence of divalent metal transporter 1 (DMT1) in neurons through increasing the expression of Ndfip1, which degrades DMT1 and does not exist in glial cells. At the same time, excess of iron increased expression of DMT1 in astrocytes and microglial cells and triggered reactive astrogliosis and microgliosis. Facing the attack of excess iron, glial cells act as neuroprotectors to accumulate more extracellular iron by upregulating DMT1, whereas neurons limit iron uptake through increasing DMT1 degradation. Cerebral accumulation of iron in animals is associated with impaired cognition, locomotion, and mood. Excess iron from surgical implants thus can affect neural cells and may be regarded as a risk factor for neurodegeneration.

scholarly journals The main impacts of COVID-19 on parkinson’s disease patients

2021 ◽  
Author(s):  
Mariana Silva Regadas ◽  
Guilherme Albuquerque de Araújo Costa ◽  
Myrela Murad Sampaio
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Risk Factor ◽  
Old Age ◽  
Neurological Diseases ◽  
Severe Form ◽  
Initial Symptom ◽  
Motor Symptoms ◽  
The Relationship ◽  
Non Motor Symptoms

Background: COVID-19 patients with chronic diseases and comorbidities are more susceptible to the severe form of the infection. Neurological symptoms are reported by some patients infected by the virus and research seeks the relationship between the virus and neurological diseases, such as Parkinson’s Disease (PD). Objectives: To understand how COVID-19 and its effects affect patients with PD. Methods: Integrative review with search on Google Scholar, Scielo, PubMed and Science Direct platforms through an online scenario, selected articles from the years 2020 and 2021. Results: SARS-CoV-2 frequently undergo mutations, causes damage and inflammation. There are reports of symptoms such as anosmia, ageusia and headache. Anosmia stands out for its relationship with one initial symptom of PD, hyposmia. As the majority of PD patients are elderly and have comorbidities, there is a higher risk of being infected. Some patients with PD infected by the virus report worsening in motor and non-motor symptoms and such worsening can occur due to systemic inflammation, stress and the measures to contain the pandemic. Conclusions: PD is not a risk factor for COVID-19, however patients may experience worsening symptoms due to comorbidities, old age and stress caused by the pandemic. Strategies that reduce stress are options for maintaining the health of patients with PD.

Iron as a risk factor in neurological diseases

ICAME 2007 ◽  
2008 ◽  
pp. 31-44
Author(s):  
Jolanta Galazka-Friedman
Keyword(s):  
Risk Factor ◽  
Neurological Diseases

scholarly journals Improved HPLC method for total plasma homocysteine detection and quantification.

2008 ◽  
Vol 55 (1) ◽  
pp. 119-126 ◽  
Author(s):  
Wojciech Sawuła ◽  
Zyta Banecka-Majkutewicz ◽  
Leszek Kadziński ◽  
Joanna Jakóbkiewicz-Banecka ◽  
Grzegorz Wegrzyn ◽  
...  
Keyword(s):  
Risk Factor ◽  
Clinical Research ◽  
Independent Risk Factor ◽  
Chromatographic Method ◽  
Neurological Diseases ◽  
Hplc Method ◽  
Plasma Homocysteine ◽  
Total Plasma ◽  
Higher Sensitivity ◽  
Detection And Quantification

Recent clinical research has pointed at hyperhomocysteinemia as an independent risk factor in a number of cardiovascular and neurological diseases. We have improved a chromatographic method of total plasma homocysteine measurements in order to obtain higher sensitivity, reliability and reproducibility. The method demonstrates excellent linearity (R=0.999), range (

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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