Characterisation of Oxidative Stress, DNA Damage and Inflammation in a Cellular Model of Parkinson’s Disease
Abstract
(ISSN 2573-4407)
OBM Neurobiology is an international peer-reviewed Open Access journal published quarterly online by LIDSEN Publishing Inc. By design, the scope of OBM Neurobiology is broad, so as to reflect the multidisciplinary nature of the field of Neurobiology that interfaces biology with the fundamental and clinical neurosciences. As such, OBM Neurobiology embraces rigorous multidisciplinary investigations into the form and function of neurons and glia that make up the nervous system, either individually or in ensemble, in health or disease. OBM Neurobiology welcomes original contributions that employ a combination of molecular, cellular, systems and behavioral approaches to report novel neuroanatomical, neuropharmacological, neurophysiological and neurobehavioral findings related to the following aspects of the nervous system: Signal Transduction and Neurotransmission; Neural Circuits and Systems Neurobiology; Nervous System Development and Aging; Neurobiology of Nervous System Diseases (e.g., Developmental Brain Disorders; Neurodegenerative Disorders).
OBM Neurobiology publishes a variety of article types (Original Research, Review, Communication, Opinion, Comment, Conference Report, Technical Note, Book Review, etc.). Although the OBM Neurobiology Editorial Board encourages authors to be succinct, there is no restriction on the length of the papers. Authors should present their results in as much detail as possible, as reviewers are encouraged to emphasize scientific rigor and reproducibility.
Publication Speed (median values for papers published in 2023): Submission to First Decision: 7.5 weeks; Submission to Acceptance: 15.9 weeks; Acceptance to Publication: 7 days (1-2 days of FREE language polishing included)
Special Issue
Oxidative Stress and Inflammatory Responses in Neurodegenerative Diseases
Submission Deadline: May 30, 2020 (Open) Submit Now
Guest Editor
Mohammad Moshahid Khan, PhD
Assistant Professor, Departments of Neurology and Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, United States
Research Interests: Neuroscience; Pharmacology; Neurodegeneration; Neuroinflammation; Parkinson’s Disease; Stroke; Alzheimer’s Disease; Multiple Sclerosis and Traumatic Brain Injury
About This Topic
Inflammation and Oxidative stress are common features of chronic neurodegenerative diseases of the central nervous system. Chronic inflammation is characterized by longstanding microglial activation followed by sustained release of inflammatory mediators, which aid in enhanced nitrosative and oxidative stress. The sustained release of inflammatory mediators propels the inflammatory cycle by increased microglial activation, promoting their proliferation and thus stimulating enhanced release of inflammatory factors. Elevated levels of several cytokines and chronic neuroinflammation have been associated with many neurodegenerative disorders of central nervous system like age-related macular degeneration, Alzheimer disease, multiple sclerosis, Parkinson’s disease, Huntington’ disease, and tauopathies. In this special issue, we aim to the introduction of the relative research the basic mechanisms of neuroinflammation and oxidative stress, the characteristics of neurodegenerative diseases, and the main immunologic responses in CNS neurodegenerative disorders. Original research reports, review articles, communications, and perspectives are welcome in all areas pertinent to the topic. All accepted papers will be published totally free of charge.
Keywords
Neurodegenerative diseases; Inflammation; Oxidative stress; Cytokines and Inflammatory factors
Planned Papers
Title: Correlation Between Neuroimaging and Epigenetics in Chronic Discogenic Lumbar Pain
Authors: M.Marchesini 1, N. Peroni 2, M. Allegri 3
Affiliation:
1. Pain Medicine Unit, ICS S. Maugeri Pavia, Italy
2. Anesthesia, Intensive Care Pain Medicine Department, San Matteo Pavia, Italy
3. Pain Therapy Service, Policlinico Monza Hospital, Monza Italy
Title: Oxydative stress and low grade inflammation in electrohypersensitivity self-reporting patients
Authors: Philippe Irigaray, Dominique Belpomme
Affiliation: Association for Research Against Cancer (ARTAC), 75015 Paris, France
Manuscript Submission Information
Manuscripts should be submitted through the LIDSEN Submission System. Detailed information on manuscript preparation and submission is available in the Instructions for Authors. All submitted articles will be thoroughly refereed through a single-blind peer-review process and will be processed following the Editorial Process and Quality Control policy. Upon acceptance, the article will be immediately published in a regular issue of the journal and will be listed together on the special issue website, with a label that the article belongs to the Special Issue. LIDSEN distributes articles under the Creative Commons Attribution (CC BY 4.0) License in an open-access model. The authors own the copyright to the article, and the article can be free to access, distribute, and reuse provided that the original work is correctly cited.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). Research articles and review articles are highly invited. Authors are encouraged to send the tentative title and abstract of the planned paper to the Editorial Office (neurobiology@lidsen.com) for record. If you have any questions, please do not hesitate to contact the Editorial Office.
Welcome your submission!
Publication
Characterisation of Oxidative Stress, DNA Damage and Inflammation in a Cellular Model of Parkinson’s Diseaseby
Alina Khan
,
Tengfei Wan
,
Catherine Hunter
,
Pavel Schweizer
,
Abbas Ishaq
,
Shobha Nagarathanam
,
Julia Morris
,
Minyu Chan
and
Gabriele Saretzki
Abstract Background: Parkinson’s disease (PD) is the second most commonly occurring neurodegenerative disease and is classed as a synucleinopathy due to the critical role of α-synuclein (α-Syn) in its pathology. α-Syn is able to translocate from the cytoplasm to the nucleus and cause DNA damage. Methods: SH-SY5Y cells were stably transfected with [...] |
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