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Pathophysiology
Published in Ibrahim Natalwala, Ammar Natalwala, E Glucksman, MCQs in Neurology and Neurosurgery for Medical Students, 2022
Ibrahim Natalwala, Ammar Natalwala, E Glucksman
TRUE – Other functions of astrocytes include angiogenesis, structural support, neural development (through migration of neurones along radial glial cells), glycogenesis, long-term potentiation, maintenance of a blood-brain barrier, removal of neurotransmitters from synapses and the conversion of glutamate to glutamine in order for neurones to reuptake glutamine.4,5
Principles of neuromotor development
Published in Mijna Hadders-Algra, Kirsten R. Heineman, The Infant Motor Profile, 2021
Mijna Hadders-Algra, Kirsten R. Heineman
Brain development also involves the creation of glial cells. Glial cell production occurs in the second half of gestation in particular. Part of the glial cells (i.e., the oligodendrocytes) take care of axonal myelination. Oligodendrocyte development peaks between 28 and 40 weeks PMA (Volpe 2009a). Myelination is prominently present in the third trimester of gestation and the first six months postnatally (Yakovlev and Lecours 1967, Haynes et al. 2005). However, myelination is a long-lasting process that is first completed around the age of 40 years (De Graaf-Peters and Hadders-Algra 2006).
Commentary
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
These reactive species, ROS and RNS, potentiate tissue damage, as well as cause oxidative and cellular injury by triggering diverse cellular pathways leading to the expression of stress-induced genes and proteins, and, in turn, produce massive injury to lipids, proteins, DNA, and biological macromolecules.6–11 Furthermore, these oxidative and nitrosative injuries potentiate glia-mediated inflammation and activation of glial cells, particularly astrocytes and microglia, at the site of injury, which leads to massive neuronal damage.9–11 Especially, the mitochondrial DNA (mtDNA) of neuronal cells is readily susceptible to structural alterations resulting in mitochondrial dysfunction.8–11 It is important to emphasize that activated glial cells are the histopathological hallmarks of neurodegenerative dysfunctions and manifestations of neuronal diseases and disorders.8–11 Multiple immune mediators, including diverse ROS, nitric oxide, proinflammatory cytokines, and chemokines, are released by activated glial cells, which are considered as noxious neurotoxins.9–11
Every nano-step counts: a critical reflection on do’s and don’ts in researching nanomedicines for retinal gene therapy
Published in Expert Opinion on Drug Delivery, 2023
Karen Peynshaert, Joke Devoldere, Stefaan De Smedt, Katrien Remaut
Besides PRs and neurons, three main types of glial cells are found in the mammalian retina: microglia, astrocytes, and Müller cells, each with distinct morphological, developmental, and antigenic characteristics. The predominant glial cell in the retina, representing 90% of all retinal glia, is the Müller cell. Müller cells are radially oriented cells, extending throughout the entire retina. They are organized in a tightly ordered pattern that allows them to come into contact with almost every cell type in the retina[4]. Finally, the retinal pigment epithelium (RPE) is a monolayer of pigmented epithelial cells, firmly packed together by tight junctions between their lateral surfaces. The RPE is located between the choroid and the outer segments of the PRs and exerts a multitude of functions. During development, the RPE is crucial for the functional differentiation of the PRs and interaction between both cell types is essential for visual function[5].
Microglia and HPA axis in depression: An overview of participation and relationship
Published in The World Journal of Biological Psychiatry, 2022
Gabriele Cheiran Pereira, Elisa Piton, Brenda Moreira dos Santos, Luis Guilherme Ramanzini, Luis Fernando Muniz Camargo, Rossano Menezes da Silva, Guilherme Vargas Bochi
The term ‘glial cells’ refers to all non-neuronal cells in the central nervous system (CNS). These cells represent over 90% of the human brain and consist of two main populations: the macroglia, represented by astrocytes and oligodendrocytes, and the microglia, the CNS tissue-resident macrophages (Greter and Merad 2013). Microglial cells detect the first signs of pathogenic invasion or tissue damage. When challenged, they can uphold tissue repair and remodelling. Paradoxically, these immune cells may also exert harmful and pathological roles in the CNS, participating in the development of psychiatric diseases (Béchade et al. 2013; Norden et al. 2015). In this context, microglial participation in the pathophysiology of depression has been suggested, mainly due to the release of proinflammatory mediators (Yirmiya et al. 2015). Emotional stress can also activate these cells and promote neuroinflammation (Kreisel et al. 2014). In addition, patients suffering from chronic inflammation are more likely to develop depressive symptoms, while depressed individuals often exhibit increased levels of circulating cytokines (Brites and Fernandes 2015). Thus, Steiner et al. (2008) demonstrated that suicidal patients with a history of depression showed morphological changes in the microglia, using post-mortem brain samples (Steiner et al. 2008).
A blend containing docosahexaenoic acid, arachidonic acid, vitamin B12, vitamin B9, iron and sphingomyelin promotes myelination in an in vitro model
Published in Nutritional Neuroscience, 2020
Jonas Hauser, Sébastien Sultan, Andreas Rytz, Pascal Steiner, Nora Schneider
The development of the brain is influenced by genetic and environmental factors. Amongst the latter, maternal and early life nutrition have been shown to play a key role in neurodevelopmental processes, such as neuronal maturation, synaptogenesis and myelination [1–3]. Myelination is the process by which oligodendrocytes (OLs), specialized glial cells in the central nervous system (CNS), form a myelin sheath around axons and this is critical for proper brain connectivity. The myelin sheath is composed of segments of condensed lipid bilayer membranes separated by the nodes of Ranvier. It increases axonal conduction velocity by reducing the capacitance of the axonal membrane and allows saltatory current [4–6]. Interestingly, brain myelination parallels the maturation of emerging cognitive functions [7]. In humans, myelination starts at mid-gestation, peaks during the first years of life and continues into adulthood [6].