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. 2019 Sep 12;9(9):99.
doi: 10.3390/bs9090099.

Neuroinflammation and Neuromodulation in Neurological Diseases

Maria de Los Angeles Robinson-Agramonte  1   2 , Carlos-Alberto Gonçalves  3 , Roberto Farina de Almeida  4 , Alina González Quevedo  5 , Sandra Chow  6 , Luis Velázquez Pérez  7 , Amado Díaz de la Fé  8 , Patricia Sesterheim  9 , Diogo Onofre Gomes Souza  3
Affiliations

Neuroinflammation and Neuromodulation in Neurological Diseases

Maria de Los Angeles Robinson-Agramonte et al. Behav Sci (Basel). .

Abstract

Neuroimmunology is a relatively young science. This discipline has emerged today from the research field as a mature and fully developed innovative research area that integrates not only pure topics of neuroimmunology, but also expands on wider fields such as neuroplasticity, neuronal reserve and neuromodulation in association with clinical events, amongst which behavioral disorders stand out. The Cuban School of Neuroimmunology-a recent meeting that took place in Havana, Cuba-focused on topics based on the molecular mechanisms of neuroinflammation in neurological disorders involving behavioral manifestations, such as multiple sclerosis (MS), autism, cerebellar ataxias, Alzheimer´s disease and stroke among others, as well as on the use of new interventional technologies in neurology. Professor Luis Velazquez, from the Cuban Academy of Sciences, dictated an interesting lecture on Spinocerebellar ataxias, a genetic disorder where recent hypotheses related to the influence of neuroinflammation as a neurobiological factor influencing the progression of this disease have emerged. At the same time, the use of new interventional technologies in neurology was discussed, including those referring to novel disease modifying therapies in the course of MS and the use of transcranial magnetic stimulation in several neurological diseases, the latter reinforcing how interventional strategies in the form of non-invasive bran stimulation can contribute to physical rehabilitation in neurology. This paper summarizes the highlights of the most relevant topics presented during the First Cuban School of Neuroimmunology, organized by the Cuban Network of Neuroimmunology, held in June 2019.

Keywords: Demyelinating disease; SCA2 Cerebellar Ataxy; Strock neurodegenerative disorders; neurodevelopmental disorders; neuroimmunology; neuroimmunomodulation; non-invasive brain stimulation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Heterogeneity of reactive astrocytes during inflammation. Astrocytes respond directly to inflammatory stimulus (e.g., via TLR4: toll like receptor 4 or indirectly to inflammatory cytokines by cytokine receptors. In basal conditions, they secrete small quantities of cytokine TNF (tumor necrosis factor) and express only TNFR1 (tumor necrosis factor receptor 1). When exposed to inflammation, TNF production is increased, as well as the expression of TNFR2, which is commonly expressed by immune cells. TNFR2-astrocytes can generate both anti-inflammatory astrocytes able to express TGF (tumor growth factor) and IL-10 and pro-inflammatory astrocytes which are able to release chemokines and attract T lymphocytes, which, in turn, release interferon gamma (IFNγ), inducing the expression of MCH class II in astrocytes, and transforming them into antigen-presenting cells.
Figure 2
Figure 2
Postulated pathways involved in GUO mechanism of action. Figure was produced with permission using Biorender free version (www.biorender.co). A1R: Adenosine a1 receptor, GLT-1: Glutamate transporter-1
Figure 3
Figure 3
Inflammation and immunity events preceding and following acute ischemic stroke.
Figure 4
Figure 4
The Evolving multiple sclerosis (MS) Treatment Landscape.
Figure 5
Figure 5
Natural history of the progression of the SCA2 cerebellar ataxia. SARA: Scale for the Assessment and Rating of Ataxia.
See this image and copyright information in PMC

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