Special Issue "Oxidative Stress and Neurodegenerative Disorders"
A special issue of Antioxidants (ISSN 2076-3921).
Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 123408
Interests: insulin signaling; insulin resistance; aging; Alzheimer’s disease; Down syndrome; neurodegeneration; mitochondrial bioenergetics
Special Issues, Collections and Topics in MDPI journals
Special Issue in International Journal of Molecular Sciences: Insulin Signaling and Fat Homeostasis in Metabolic and Neurodegenerative Disorders
Special Issue in Antioxidants: Crosstalk between Cell Redox Homeostasis and Synaptic Functions in Physiological and Pathological Conditions
Increased oxidative stress levels have been found to greatly contribute to the onset and progression of neurodegenerative disorders, i.e., Alzheimer’s disease, Parkinson’s disease, Down syndrome, and Huntington disease. Loss of physiological equilibrium between antioxidant and pro-oxidant stimuli, which normally contribute to the maintenance of low free radical levels, leads to increased generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) that are toxic for brain cells in several ways. Indeed, augmented ROS/RNS production is responsible for proteins, lipids, and nucleic acids damage, which accumulates within the cells and disrupts cellular homeostasis. Perturbation of mitochondrial activity further boosts ROS/RNS production, finally resulting in impaired metabolic pathways normally fueling brain cells’ energetic needs. In that frame, neurons display a distinctive bioenergetic metabolism, and the mitochondrial oxygen consumption rate is particularly elevated to sustain the high ATP (energy) expenditure. These features contribute to the exquisite sensitivity of the brain to the detrimental effects of oxidative stress. Recent findings suggest the crucial role of metabolic networks in the regulation of neuronal tolerance against oxidative stress. Furthermore, emerging evidence highlights the impact of metabolism and redox signaling on genetic and epigenetic regulation of gene expression. Collectively, these elements indicate the extraordinary complexity of the multileveled molecular mechanisms deployed by brain cells to cope with oxidative stress.
This research topic will discuss preclinical and clinical evidence highlighting the central role of oxidative stress in the progression of neurodegenerative disorders and which are current strategies adopted to protect the brain.
Prof. Dr. Eugenio Barone
Prof. Dr. Marzia Perluigi
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- Oxidative stress
- Brain metabolism
- Alzheimer disease
- Parkinson disease
- Down syndrome
- Huntington disease