Special Issue "Neuroinflammation in Neurodegenerative and Neurological Diseases"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 May 2020.

Special Issue Editor

Dr. Vicente Felipo
E-Mail Website
Guest Editor
Laboratory of Neurobiology, Centro de Investigación Príncipe Felipe, Valencia, Spain
Interests: neuroinflammation; neurotransmission; hepatic encephalopathy; hyperammonemia; cognitive impairment; motor alterations

Special Issue Information

Dear Colleagues,

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
Guest Editor

Manuscript Submission Information

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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.


  • neuroinflammation;
  • immune system-CNS cross talk;
  • neurological impairment;
  • glial activation;
  • mediators of inflammation: chemokines, interleukins, and extracellular vesicles.

Published Papers (1 paper)

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Open AccessFeature PaperArticle
Characterization of Mesenchymal Stem Cells Derived from Patients with Cerebellar Ataxia: Downregulation of the Anti-Inflammatory Secretome Profile
Cells 2020, 9(1), 212; https://doi.org/10.3390/cells9010212 - 15 Jan 2020
Mesenchymal stem cell (MSC) therapy is a promising alternative approach for the treatment of neurodegenerative diseases, according to its neuroprotective and immunomodulatory potential. Despite numerous clinical trials involving autologous MSCs, their outcomes have often been unsuccessful. Several reports have indicated that MSCs from [...] Read more.
Mesenchymal stem cell (MSC) therapy is a promising alternative approach for the treatment of neurodegenerative diseases, according to its neuroprotective and immunomodulatory potential. Despite numerous clinical trials involving autologous MSCs, their outcomes have often been unsuccessful. Several reports have indicated that MSCs from patients have low capacities in terms of the secretion of neurotrophic or anti-inflammatory factors, which might be associated with cell senescence or disease severity. Therefore, a new strategy to improve their capacities is required for optimal efficacy of autologous MSC therapy. In this study, we compared the secretory potential of MSCs among cerebellar ataxia patients (CA-MSCs) and healthy individuals (H-MSCs). Our results, including secretome analysis findings, revealed that CA-MSCs have lower capacities in terms of proliferation, oxidative stress response, motility, and immunomodulatory functions when compared with H-MSCs. The functional differences were validated in a scratch wound healing assay and neuron-glia co-cultures. In addition, the neuroprotective and immunoregulatory protein follistatin-like 1 (FSTL1) was identified as one of the downregulated proteins in the CA-MSC secretome, with suppressive effects on proinflammatory microglial activation. Our study findings suggest that targeting aspects of the downregulated anti-inflammatory secretome, such as FSTL1, might improve the efficacy of autologous MSC therapy for CA. Full article
(This article belongs to the Special Issue Neuroinflammation in Neurodegenerative and Neurological Diseases)
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