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Regulation of Glial Function by Insulin Peptides
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Ana M. Fernandez, Laura Martinez-Rachadell, Patricia Miranda-Azpiazu, Ignacio Torres Aleman
Demyelinating diseases are of high clinical impact (92). Unfortunately, none of them still have a cure. As a regenerative factor, IGF-I was shown time ago to participate in re-myelinating responses to various types of central injuries (93, 94), although these observations were not confirmed by others (95). Evidence indicated that astrocyte-derived IGF-I participates in re-myelinating responses to injury (96). Just recently, IGF-I, together with insulin, has been shown to be required in homeostatic reactivity to peripheral neuropathies, acting through Schwann cells (91). Despite its protective actions in pre-clinical demyelinating models, a pilot study in multiple sclerosis patients did not show changes in the disease course (97). Thus, as with most potential clinical uses of ILPs in the diseased brain, the therapeutic utility of IGF-I in demyelinating diseases has not been further pursued.
Non-traumatic neurological conditions in medico-legal work
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
This is the most common form of demyelinating disease. It is a relapsing-remitting disorder in which plaques of demyelination can be widely distributed throughout the CNS. In general, the forensic pathologist will encounter multiple sclerosis (MS) as an incidental finding rather than a direct cause of death, although death may occur if there is acute demyelination in the brainstem. In chronic MS, the plaques have a predilection for subependymal (periventricular) and subpial sites, and for the cortical grey-white matter junction. Chronic plaques are sunken and grey and generally sharply defined. Acute plaques have a rather more granular appearance (Figure 18.11). The optic nerves should be examined if possible.
Neuroinfectious Diseases
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Jeremy D. Young, Jesica A. Herrick, Scott Borgetti
Potential chronic neurologic complications of COVID-19Cognitive function. Approximately one-third of hospitalized COVID-19 patients with severe clinical features who are subsequently discharged have deficits in executive function.4 The long-term outcomes for these patients are not clear. It also is unknown whether these patients are at risk for the development of a progressive dementia similar to that observed in HIV/AIDS.29Demyelinating disease. In experimental animal models, coronaviruses initiate the formation of CNS demyelinating lesions similar to those seen in multiple sclerosis.30 At this point in time, there has not been a reported increase in MS-like diseases in patients who have recovered from COVID-19. However, assessment of the long-term impact of COVID-19 on the development of neurologic and autoimmune diseases will require clinical monitoring over several years.
Neuropsychiatric manifestations in primary Sjogren syndrome
Published in Expert Review of Clinical Immunology, 2022
Simone Appenzeller, Samuel de Oliveira Andrade, Mariana Freschi Bombini, Samara Rosa Sepresse, Fabiano Reis, Marcondes C. França
Definitions for neuropsychiatric manifestations, including a minimal set of investigation and attribution criteria, are the first step toward a standardization. Positive experience has been made in other autoimmune diseases, such as systemic lupus erythematosus. Therefore, we consider that an international, multidisciplinary study could significantly contribute and make an important step toward diagnostic and/or classification criteria for neuropsychiatric manifestations in pSS. So far, these have been classified as PNS, CNS (Diffuse, focal, and spinal cord involvement), and ANS. Some manifestations, such as demyelinating disease, have to be differentiated from multiple sclerosis and neuromyelitis optica. Definition criteria and attribution could significantly impact future studies allowing comparisons of different cohorts and validation of biomarkers.
Are electrophysiological and oligodendrocyte alterations an element in the development of multiple sclerosis at the same time as or before the immune response?
Published in International Journal of Neuroscience, 2021
Genaro Gabriel Ortiz, Mario A. Mireles-Ramírez, Fermín P. Pacheco-Moisés, Luis J. Ramírez-Jirano, Oscar K. Bitzer-Quintero, Daniela L. C. Delgado-Lara, L. Javier Flores-Alvarado, Miriam A. Mora-Navarro, Miguel Huerta, Blanca M. G. Torres-Mendoza
Multiple Sclerosis (MS) is defined as an inflammatory disease of the white matter (myelin). The central nervous system is mediated by autoreactive clones of T cells that would act against antigens (autoantigens) of myelin, causing their destruction, which would condition the symptomatology and appearance of the dysfunction. Multiple sclerosis is considered a disease mediated by helper T lymphocytes (CD4), but this fact, far from being proven, presents too much evidence that puts it in doubt as to the primary mechanism of the disease [1–3]. The disorder is diagnosed most often between 20 and 40 years of age but can be seen at any age. Multiple sclerosis is caused by damage to the myelin sheath, which is the protective covering that surrounds neurons. Damage to the nerve is caused by inflammation that occurs when the body's immune cells attack the nervous system, which can occur along any area of the brain, the optic nerve, or the spinal cord (among others). The clinical picture of MS is a consequence of the anatomopathological lesions observed in the central nervous system: inflammation, demyelination, axonal degeneration and gliosis, and their electrophysiological consequences such as conduction blocks, axonal hyperexcitability, and the generation of ectopic potentials [4–7]. There is no simple explanation with the most classic theories, and it is suggested that it is a demyelinating disease almost exclusively (Table 1).
Emerging myelin repair agents in preclinical and early clinical development for the treatment of multiple sclerosis
Published in Expert Opinion on Investigational Drugs, 2020
Stefan Gingele, Martin Stangel
Multiple sclerosis (MS) is a chronic autoimmune-mediated disease of the central nervous system (CNS) in which inflammation-driven demyelination represents the pathological core [1]. Myelin and myelin-forming oligodendrocytes are essential for the maintenance of normal axonal function and survival since they provide important trophic support for the axon and enable fast saltatory impulse conduction. Demyelination is therefore considered to result in axonal damage and loss which is thought to be responsible for progressive clinical disability [2,3]. However, it has to be kept in mind that axonal injury in demyelinating diseases can arise from various reasons apart from demyelination itself. Among other things, the omission of the myelin sheath as a physical barrier against autoreactive cytotoxic T cells, nitric oxide, metalloproteinases, and other inflammatory mediators produced by microglia and astrocytes is toxic to axons. Furthermore, increased energy demand in response to demyelination-related ion-channel redistribution along the axon together with axonal mitochondrial dysfunction can lead to a state of ‘virtual hypoxia’ resulting in increased intra-axonal Ca2+ concentration, glutamate excitotoxicity, and consecutive axon loss [1,2].