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<title>Enfermedades Desmielinizantes.capítulo de libro</title>
<link href="https://repositorio.fleni.org.ar/xmlui/handle/123456789/1220" rel="alternate"/>
<subtitle/>
<id>https://repositorio.fleni.org.ar/xmlui/handle/123456789/1220</id>
<updated>2026-04-04T08:43:08Z</updated>
<dc:date>2026-04-04T08:43:08Z</dc:date>
<entry>
<title>Chapter 10 - Autoimmune Astrocytopathy</title>
<link href="https://repositorio.fleni.org.ar/xmlui/handle/123456789/1322" rel="alternate"/>
<author>
<name>Correale, Jorge</name>
</author>
<id>https://repositorio.fleni.org.ar/xmlui/handle/123456789/1322</id>
<updated>2025-03-17T14:52:06Z</updated>
<published>2024-01-01T00:00:00Z</published>
<summary type="text">Chapter 10 - Autoimmune Astrocytopathy
Correale, Jorge
Astrocytes constitute the most abundant type of glial cells in the central nervous system (CNS) and display significant heterogeneity. Astrocytes actively engage in various metabolic processes and are active contributors to immune responses within the CNS, with either beneficial or detrimental outcomes. The dynamic response of astrocytes to external signals leads to alterations in morphology, molecular expression, and function. In addition, autonomous cell-driven changes in innate properties may contribute to various autoimmune and neurodegenerative diseases.&#13;
&#13;
The development of neuromyelitis optical spectrum disorder (NMOSD) is determined by pathogenic antibodies targeting the water channel aquaporin-4 (AQP4) located in astrocyte end feet. AQP4-IgG facilitates the differential diagnosis of NMOSD. Similarly, a newly identified autoantibody against GFAP serves as a biomarker for a relapsing autoimmune form of meningoencephalomyelitis, responsive to steroids and often associated with tumors. In Rasmussen’s encephalitis, CD8+ T lymphocytes induce astrocyte loss in affected areas, disrupting normal neuronal function. Additionally, astrocytes mediate multiple mechanisms involved in the genesis and progression of multiple sclerosis (MS) and remyelination processes. Finally, reactive astrocytes play a crucial role in various CNS infections, both during acute phases and in the long term, influencing the development of post-infectious sequelae. These observations underscore the active participation of astrocytes in both pathological and repair mechanisms observed in CNS immune-mediated diseases. Characterizing the cellular and molecular mechanisms underlying astrocyte pathophysiology represents a new frontier to identify novel therapeutic strategies for CNS pathologies.
</summary>
<dc:date>2024-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Chapter 2 - Novel imaging approaches in multiple sclerosis.</title>
<link href="https://repositorio.fleni.org.ar/xmlui/handle/123456789/1230" rel="alternate"/>
<author>
<name>Farez, Mauricio Franco</name>
</author>
<id>https://repositorio.fleni.org.ar/xmlui/handle/123456789/1230</id>
<updated>2024-10-29T14:52:17Z</updated>
<published>2024-01-01T00:00:00Z</published>
<summary type="text">Chapter 2 - Novel imaging approaches in multiple sclerosis.
Farez, Mauricio Franco
In recent years, there has been significant advancement in the utilization of magnetic resonance imaging (MRI) for the diagnostic evaluation of patients with multiple sclerosis (pwMS). The 2017 McDonald criteria have demonstrated high sensitivity and accuracy in predicting a second clinical attack in patients with a typical clinically isolated syndrome, enabling earlier diagnosis of Multiple Sclerosis (MS) (Thompson et al. (2018). Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. The Lancet Neurology, 17(2), 162–173). These criteria have been validated and are supported by evidence, simplifying the clinical application of MRI criteria and enhancing the management of MS patients. However, in order to minimize the risk of misdiagnosis, these criteria should only be applied by expert clinicians after thorough exclusion of alternative diagnoses (Filippi et al. (2023). Present and future of the diagnostic work-up of multiple sclerosis: The imaging perspective. Journal of Neurology. 270(3), 1286–1299), a task that often is not easy. Thus, several imaging methods are currently being developed or studied and are the goal of this chapter.
</summary>
<dc:date>2024-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Chapter 3 - Effect of infections on multiple sclerosis</title>
<link href="https://repositorio.fleni.org.ar/xmlui/handle/123456789/1221" rel="alternate"/>
<author>
<name>Correale, Jorge</name>
</author>
<author>
<name>Marrodán, Mariano</name>
</author>
<id>https://repositorio.fleni.org.ar/xmlui/handle/123456789/1221</id>
<updated>2024-10-22T16:38:20Z</updated>
<published>2024-01-01T00:00:00Z</published>
<summary type="text">Chapter 3 - Effect of infections on multiple sclerosis
Correale, Jorge; Marrodán, Mariano
Evidence from both epidemiological and experimental studies, implicate infections present during childhood and young adulthood to the development and/or exacerbation of MS. Possible infectious agents include Epstein–Barr virus, human Herpesvirus-6, human endogenous retrovirus families, and coronavirus. In addition, common upper respiratory tract, gastrointestinal and urogenital tract bacterial infections have also been associated with MS exacerbations. In contrast, helminth infections appear to attenuate the course of MS, with effects extending beyond simple response to an infectious agent. Although the cause of MS in humans remains inconclusive, an infectious etiology is one possibility, as microbial agents may modulate the immune system in genetically susceptible individuals. Decoding the complex interaction between central nervous system cells, infections caused by various pathogens, and the immune response to those infections may improve our understanding of pathogenic mechanisms present in MS, and help develop new treatment strategies and/or prevent relapses.
</summary>
<dc:date>2024-01-01T00:00:00Z</dc:date>
</entry>
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