alexa Mitochondrial Dysfunction And Neuronal Redox Imbalance - The Primary Cause Of Rett Syndrome?
ISSN: 2155-9562

Journal of Neurology & Neurophysiology
Open Access

Like us on:
OMICS International organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations

700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)

Share This Page

Additional Info

Loading
Loading Please wait..
 

Joint Conference 12th International Conference on Neurology and Neurophysiology & 2nd International Conference and Exhibition on Dual Diagnosis
May 18-20, 2017 Munich, Germany

Karolina Can
University in Göttingen, Germany
ScientificTracks Abstracts: J Neurol Neurophysiol
DOI: 10.4172/2155-9562-C1-049
Abstract
Statement of the Problem: Rett syndrome (RTT) is a neurodevelopmental disorder, which occurs almost exclusively in girls with a prevalence of 1:10.000-1:15.000 life births. The genetic causes of RTT are de novo mutations in the MECP2 gene. After a short normal development, developmental stagnation occurs with a neuronal and autonomic dysfunction, manifested as mental retardation, erratic breathing, epilepsy, loss of speech and stereotypical hand movements. Growing evidence indicates that RTT associates with mitochondrial dysfunction and oxidative stress. We previously showed that mitochondria of MeCP2-deficient (Mecp2-/y) mouse hippocampus are partly uncoupled and show a higher consumption of O2. To assess molecular events contributing to redox impairment, we intensified our analyses focusing specifically on neurons and their cytosolic and mitochondrial compartments. Methodology & Theoretical Orientation: Quantitative real-time imaging of redox dynamics was performed with the geneticallyencoded redox sensor roGFP1 in cytosol and mitochondrial matrix of dissociated neurons and organotypic hippocampal slices. Optimized expression was achieved by viral transduction. Findings: Detailed excitation ratiometric fluorescence microscopy confirmed that in Mecp2-/y hippocampal neurons, the redox imbalance affects the cytosolic and mitochondrial compartments. These changes were especially obvious for more complex organotypic slices. Redox challenge by H2O2 and severe hypoxia elicited intensified oxidizing and reducing transients in Mecp2-/y neurons, respectively. Inhibition of superoxide dismutase elicited only a dampened oxidation in Mecp2-/y cytosol and mitochondria, suggesting a decreased efficiency of this scavenging enzyme in Rett mice. More importantly, stimulation by neurotransmitters consistently evoked intensified oxidizing shifts in the cytosol of Mecp2-/y neurons. Conclusions & Significance: Redox imbalance associated with RTT clearly affects cytosol and mitochondria of central neurons. Even physiological events such as neurotransmitter stimulation are sufficient to provoke overshooting redox responses in Mecp2-/y neurons. As these changes are already evident in presymptomatic mice, they may promote the progression of RTT.
Biography

Karolina Can is a Post-Doctoral Researcher, whose expertise focuses on Rett syndrome and oxidative stress. She performed her PhD at the Georg-August University in Göttingen in Germany, where she now continues running various projects towards mitochondrial dysfunction and potential molecular targets involved in this neurodevelopmental disorder. She strictly extended her proficiency already during her Master’s studies (MSc performed at Jagiellonian University in Krakow in Poland), when she took advantage on annual internship in the Institute of Human Genetics in Göttingen in Germany, and switched her gears from genetics towards neurophysiology and live-cell imaging.

Email: karolina.can@gmail.com

image PDF   |   image HTML
 

Relevant Topics

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri, Food, Aqua and Veterinary Science Journals

Dr. Krish

agrifoodaquavet@omicsonline.com

1-702-714-7001 Extn: 9040

Clinical and Biochemistry Journals

Datta A

clinical_biochem@omicsonline.com

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

business@omicsonline.com

1-702-714-7001Extn: 9042

Chemical Engineering and Chemistry Journals

Gabriel Shaw

chemicaleng_chemistry@omicsonline.com

1-702-714-7001 Extn: 9040

Earth & Environmental Sciences

Katie Wilson

environmentalsci@omicsonline.com

1-702-714-7001Extn: 9042

Engineering Journals

James Franklin

engineering@omicsonline.com

1-702-714-7001Extn: 9042

General Science and Health care Journals

Andrea Jason

generalsci_healthcare@omicsonline.com

1-702-714-7001Extn: 9043

Genetics and Molecular Biology Journals

Anna Melissa

genetics_molbio@omicsonline.com

1-702-714-7001 Extn: 9006

Immunology & Microbiology Journals

David Gorantl

immuno_microbio@omicsonline.com

1-702-714-7001Extn: 9014

Informatics Journals

Stephanie Skinner

omics@omicsonline.com

1-702-714-7001Extn: 9039

Material Sciences Journals

Rachle Green

materialsci@omicsonline.com

1-702-714-7001Extn: 9039

Mathematics and Physics Journals

Jim Willison

mathematics_physics@omicsonline.com

1-702-714-7001 Extn: 9042

Medical Journals

Nimmi Anna

medical@omicsonline.com

1-702-714-7001 Extn: 9038

Neuroscience & Psychology Journals

Nathan T

neuro_psychology@omicsonline.com

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

John Behannon

pharma@omicsonline.com

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

social_politicalsci@omicsonline.com

1-702-714-7001 Extn: 9042

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
adwords