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As the aged population more enlarges, the age-related health disorders are increasing, including neurological disorders. The economic burden of care and treatment of neurological disorders also increase. It is an urgent challenge to prevent or even reverse neurological disorders. More special attention has been paid to the clinical and experimental research in neurological disorders worldwide. Thus, Clinical and Experimental Neurology will offer an academic and professional platform for medical scientific community to discover the more mechanisms for neurological disorders, and benefit the combat for the prevention and treatment of neurological disorders.

ISSN (Print): 2379-7789

ISSN (Online): 2379-7797

Editor-in-Chief: Zhiyou Cai, MD

Website: http://www.sciepub.com/journal/IJCEN



Epigenetic Study of Parkinson’s Disease in Experimental Animal Model

1Biochemistry Section, Department of Chemistry

2Department of medical Biochemistry, Faculty of Medicine, Tanta University

3Department of Zoology, Faculty of Science

4Department of Zoology, Faculty of Science, Minoufiya University, Egypt

International Journal of Clinical and Experimental Neurology. 2015, 3(1), 11-20
doi: 10.12691/ijcen-3-1-3
Copyright © 2015 Science and Education Publishing

Cite this paper:
Afrah F Salama, Wafaa Ibrahim, Ehab Tousson, Saber Sakr, Ahmed Masoud, Mohamed A Akela, Mahmoud A. Abd El-Rahman. Epigenetic Study of Parkinson’s Disease in Experimental Animal Model. International Journal of Clinical and Experimental Neurology. 2015; 3(1):11-20. doi: 10.12691/ijcen-3-1-3.

Correspondence to: Ehab  Tousson, Department of Zoology, Faculty of Science. Email: toussonehab@yahoo.com


Epigenetic modifications are defined as mechanisms that are able to modify the expression levels of selected genes without necessarily altering their DNA sequence, as histone tail modifications. These modifications are likely to contribute to the onset and progression of complex human diseases including neurodegenerative ones. Oxidative stress also is thought to be a common underlying mechanism that leads to cellular dysfunction and demise in PD. This study was aimed to assess the epigenetic fingerprint in PD experimental model through HDAC, PARP and activities oxidative stress markers. Materials and methods: The study was carried out on five rat groups, control group, Parkinsonism group, sodium butyrate group, two parkinson’s disease groups co-treated and post treated with sodium butyrate. Parkinsonism was induced by ip injection of paraquat. Laboratory measurements included serum 8-OHdG, MDA level as biomarkers of oxidative stress. HDAC and PARP activities were measured as other epigenetic mechanisms. Results: PD group, PD co-treated and post treated with sodium butyrate showed significant increase in HDAC and PARP activities. Also, there was significant increase in serum 8-OHdG level and MDA level in both serum and tissue. Conclusion and recommendations: The increments in HDAC and PARP activities are either two of the pathogenic mechanisms of the disease or it affords PD patients neuroprotection and benefits. Also, sodium butyrate is one of best antioxidant and neuroprotective agents. We recommended for further studies in HDAC and sodium butyrate as inhibitor in neurodegerative diseases, other diseases and normal state.



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Neuroprotective Role of Vitamin B3 in Experimentally Induced Oxidative Stress

1Zoology Department, Faculty of Science

2Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta 31527, Egypt

International Journal of Clinical and Experimental Neurology. 2015, 3(1), 21-25
doi: 10.12691/ijcen-3-1-4
Copyright © 2015 Science and Education Publishing

Cite this paper:
Afaf El Atrash, Lamees Dawood, Ehab Tousson, Amira Salama. Neuroprotective Role of Vitamin B3 in Experimentally Induced Oxidative Stress. International Journal of Clinical and Experimental Neurology. 2015; 3(1):21-25. doi: 10.12691/ijcen-3-1-4.

Correspondence to: Ehab  Tousson, Zoology Department, Faculty of Science. Email: oussonehab@yahoo.com


Paraquat is a widely used herbicide. The main mechanism underlying PQ toxicity is oxidative stress. Niacin (nicotinic acid) a precursor for NAD+ It has also been reported to possess oxygen radical scavenging activity. The enzyme PARP-1 is activated by DNA strand breaks, using NAD+ as a substrate. Thus, the present study aimed to assess the magnitude of oxidative DNA damage and the role of PARP and the advantages of modulating its activity by niacin supplementation in experimentally induced oxidative stress by PQ. 50 male albino rats were equally divided into five groups; the first and second groups were the control and PQ treated groups respectively while the 3rd group was nicotinic acid treated group; the 4th and 5th groups were co- and post treated PQ treated rats with nicotinic acid respectively. Serum 8-hydroxy-2'-deoxyguanosine and brain MDA levels in PQ treated group showed a significant increase when compared with control group, while levels of PARP activity and TAC in PQ treated group showed a significant decrease when compared with control group. A significant increase of PARP activity & TAC and a significant decrease in serum 8-hydroxy-2'-deoxyguanosine&MDA after nicotinic acid injection when compared with control group was observed. Post-treatment with nicotinic acid improved the biochemical and histopathological alterations in brain treated with nicotinic acid, while co-treatment with nicotinic acid protected against ROS production.



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Cyclooxygenase Expression in Canines Following Peripheral Nerve Injury

1Department of Orthopedics and Rehabilitation Medicine, Faculty of Medical Sciences, The University of Fukui, Fukui, Japan

2Research and Education Program for Life Science, The University of Fukui, Fukui, Japan

3Department of Orthopedic Surgery, Suzuki Orthopaedic Clinics, Toki, Gifu, Japan

4Department of Orthopedic Surgery, Yamada Orthopaedic Clinics, Hamamatsu, Shizuoka, Japan

5Victor Horsley Department of Neurosurgery, The National Hospital for Neurology and Neurosurgery, Queen Square, London, UK

International Journal of Clinical and Experimental Neurology. 2015, 3(2), 26-31
doi: 10.12691/ijcen-3-2-1
Copyright © 2015 Science and Education Publishing

Cite this paper:
Shigeru Kobayashi, Yoshihiko Suzuki, Syuichi Yamada, Naji Al-Khudairi, Adam Meir. Cyclooxygenase Expression in Canines Following Peripheral Nerve Injury. International Journal of Clinical and Experimental Neurology. 2015; 3(2):26-31. doi: 10.12691/ijcen-3-2-1.

Correspondence to: Shigeru  Kobayashi, Department of Orthopedics and Rehabilitation Medicine, Faculty of Medical Sciences, The University of Fukui, Fukui, Japan. Email: kshigeru@u-fukui.ac.jp


In order to investigate the mechanism of neurogenic pain, this study used a median nerve compression model in dogs. The nerve was compressed with a clip for three weeks. Immunohistochemistry was done by the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against cyclooxygenase (COX)-1 and 2 were used to examine the localization and changes of these mediators caused by nerve compression. In control animals, resident T cells were detected, but there were no macrophages. COX-2 was positive in the Schwann cells and vascular endothelial cells, while COX-1 was detected in the vascular endothelial cells. After nerve compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for COX-2. COX-2 may be deeply involved in neuritis arising from mechanical compression, and this mediator seems to be important in the manifestation of neurogenic pain.



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