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Special Issue "Neuroinflammation in Neurodegenerative and Neurological Diseases"
Deadline for manuscript submissions: 31 May 2020.
Chronic neuroinflammation plays a main role in neurodegenerative diseases, including Alzheimer’s and Parkinson’s diseases and multiple sclerosis, and in other neurological diseases such as schizophrenia, stroke, and hepatic encephalopathy. Neuroinflammation also arises in many pathologies associated with chronic inflammation (such as diabetes and rheumatoid arthritis), which are not traditionally considered as neurological diseases but may also lead to impairment of cognitive and motor function, depression, and other alterations of cerebral function that are mediated by neuroinflammation.
This pathological neuroinflammation is mainly mediated by microglia and astrocytes, which play important immunomodulatory functions in the brain. Neuroinflammation alters the communication between cells in the CNS and leads to altered neurotransmission, which alters cognitive and motor functions and may also led to depression and other deleterious consequences.
Alterations in the peripheral immune system play a key role in the induction of neuroinflammation. There are different mechanisms by which these peripheral changes may be transmitted to the brain, which may or may not involve infiltration into the brain of cells of the peripheral immune system.
This Special Issue welcomes original papers and reviews on any relevant aspect of the mechanisms involved in the induction of neuroinflammation in neurodegenerative and other neurological diseases: the role of microbiota and the gut–brain axis; how peripheral inflammation is transmitted to the brain; the role of cells of the immune system, of endothelial cells and of microglia, of astrocytes and other brain cells, and of the mediators in the communication between these cells (cytokines, chemokines, their receptors, extracellular vesicles including exosomes, etc.); and the molecular mechanisms of the activation of microglia and astrocytes.
Studies on how neuroinflammation alters neurotransmission and leads to cognitive and motor impairment, depression, or other deleterious consequences are also welcome.
New therapeutic approaches to restore these neurological alterations by acting on any target of any step of the processes by which peripheral inflammation leads to neuroinflammation are welcome; how neuroinflammation alters neurotransmission or induces neurodegeneration and how this induces depression or impairment of cognitive and motor function will be also considered.
Dr. Vicente Felipo
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 papers will be 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. Cells 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 2000 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.
- immune system-CNS cross talk;
- neurological impairment;
- glial activation;
- mediators of inflammation: chemokines, interleukins, and extracellular vesicles.