China
Africa
Explore chapters and articles related to this topic
Role of Tandem Mass Spectrometry in Diagnosis and Management of Inborn Errors of Metabolism
Published in P. Mereena Luke, K. R. Dhanya, Didier Rouxel, Nandakumar Kalarikkal, Sabu Thomas, Advanced Studies in Experimental and Clinical Medicine, 2021
Kannan Vaidyanathan, Sandhya Gopalakrishnan
Fogli et al. used MALDI-TOF/MS to analyze CSF N-glycan profile and they suggest that this can be used to study leukodystrophies arising due to eIF2B mutations. They suggest that the method could also be extended to study other neurological disorders involving developmental gliogenesis/synaptogenesis abnormalities [56].
Drugs in pregnancy and lactation
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Post-mortem exams of infants exposed in utero to ethanol can show reduced brain weight and disturbances of the horizontal cortical lamination, neuronal ectopias (sometimes invading the meninges) and/or a reduced thickness of the cortical mantle. Several mechanisms underlying the effects of ethanol on the developing brain have been unravelled in animal models (Table 2): i) ethanol stimulates GABA-A receptors and inhibits the glutamatergic N-methyl-D-aspartate receptor, two key receptors in multiple steps of brain development [8,9], acute ethanol administration has also been shown to interfere with other systems of neurotransmitters including serotonin, dopamine and neuropeptide Y,ii) ethanol inhibits the proliferation of neuronal precursors, impairs their migration and induces excess neuronal cell death [10–13],iii) ethanol also disturbs several critical steps of neocortical gliogenesis [10,12], leading to abnormalities in neuronal function, neuronal survival and cerebral cytoarchitectonics.
Neural Stem Cells and Oligodendrocyte Progenitors in the Central Nervous System
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Jennifer A. Jackson, Diana L. Clarke
All cells comprising the CNS are originally derived from the early neuroepithelium that forms as the neural plate along the midline of the developing embryo. As development proceeds, this single layer of pseudostratified epithelium folds to form the neural tube (Fig. 1). The differentiation of the neuroepithelial stem cells into neurons and glia then proceeds in a temporal specific manner that is specific for each region of the developing neural tube.4,5 Generally neurogenesis occurs first, followed by gliogenesis. This patterning of the neural tube is thought to begin at the neural plate stage of development through inductive interactions that create organizing centers at the dorsal and ventral poles.6-8 These specialized neuroepithelial cells generate signals that induce, often in a concentration dependent manner, the expression of patterning genes in adjacent neuroepithelial cells. These patterning genes generally encode homeodomain transcription factors, and their expression patterns divide the cells in the neuroepithelium into different domains along the rostral-caudal and dorso-ventral axes of the neural tube.9,10 These patterning genes are thought to specify neuronal subtype identity and control the duration of specific types of neurogenesis occurring in the brain and spinal cord during each developmental stage.
Undernutrition – thirty years of the Regional Basic Diet: the legacy of Naíde Teodósio in different fields of knowledge
Published in Nutritional Neuroscience, 2022
Larissa B. Jannuzzi, Amaury Pereira-Acacio, Bruna S. N. Ferreira, Debora Silva-Pereira, João P. M. Veloso-Santos, Danilo S. Alves-Bezerra, Jarlene A. Lopes, Glória Costa-Sarmento, Lucienne S. Lara, Leucio D. Vieira, Ricardo Abadie-Guedes, Rubem C.A. Guedes, Adalberto Vieyra, Humberto Muzi-Filho
Besides neurons, it became clear in the late nineties that glial cells could be affected by undernutrition and that RBD might again be useful. Mendonça et al. [28] investigated the effects of RBD-provoked undernutrition in young rats (in utero and during lactation) on the astrocyte distribution in 2 hypothalamic regions, the circadian pacemaker suprachiasmatic nucleus (SCN) and the medial preoptic area (MPA), which control the formation and physiology of astrocytes. Glial fibrillary acidic protein (GFAP) expression is reduced in SCN and MPA from undernourished rats, which suggests that undernutrition in the 2 development periods led to alterations in gliogenesis or glial cell proliferation in both nuclei, with an influence on neuronal development and function as a whole [29]. Furthermore, compensatory plasticity mechanisms in GFAP expression seem to be developed in astrocyte differentiation in the SCN, especially when undernutrition occurred during lactation [28], demonstrating that cellular loss induced by undernutrition stimulates these compensatory mechanisms, thereby unveiling one of the most important defenses ensuring survival under adverse conditions.
The effects of glial cells inhibition on spatial reference, reversal and working memory deficits in a rat model of traumatic brain injury (TBI)
Published in International Journal of Neuroscience, 2022
Amir Rezagholizadeh, Seyed Asaad Karimi, Narges Hosseinmardi, Mahyar Janahmadi, Mohammad Sayyah
Two of the common and debilitating symptoms experienced by TBI survivors are memory impairments and reduced seizure thresholds (6). Many studies have shown that glial cells play an important role in cognitive functions such as learning and memory (7). Also, it has been reported that glial cells also play essential roles in regulation of synaptogenesis, formation of the scaffold around the nervous system, regulation of cerebral microcirculation, control of the CNS microenvironment, regulation of extracellular ion concentrations; in particular sequestration and redistribution of potassium ion, removal of neurotransmitters from the extracellular space, control of the brain water homeostasis, collecting neuronal waste, regulation of neurogenesis and gliogenesis, and integration of neuronal–glial networks (8). Moreover, glial cells especially astrocytes participate in synaptic plasticity that is believed to be the cellular basis for learning and memory (9).
Gene and protein expression profiles of JAK-STAT signalling pathway in the developing brain of the Ts1Cje down syndrome mouse model
Published in International Journal of Neuroscience, 2019
Han-Chung Lee, Hadri Hadi Md Yusof, Melody Pui-Yee Leong, Shahidee Zainal Abidin, Eryse Amira Seth, Chelsee A. Hewitt, Sharmili Vidyadaran, Norshariza Nordin, Hamish S. Scott, Pike-See Cheah, King-Hwa Ling
The manifestation of various pathological features in the DS brain could in part be attributed to defective neurogenesis and a reduction of neuronal number in several brain regions. The proportion of neurons in DS foetuses is significantly lower in the dentate gyrus, hippocampus and parahippocampal gyrus compared to healthy controls [4]. Moreover, the precursor cells for cerebellar neurons, which originate from the external granular layer and ventricular zone, also show impaired proliferation [5]. DS neural progenitors have greater tendency to differentiate into glial cells, as demonstrated by studies that used glial fibrillary astrocyte protein (GFAP) as a marker. GFAP-stained positive cells were increased in the hippocampus of post-mortem DS foetal brains, [4] as well as in neurospheres derived from human DS-induced pluripotent stem cells (iPSCs) [6]. An increase in GFAP expression was also seen in proliferating neurospheres derived from embryonic Ts1Cje mouse brain [7] with a greater number of astrocytes compared to wild-type mice upon differentiation [8]. The neural progenitor pool that favours astrocytic differentiation may affect the normal development and function of the brain. Therefore, understanding the changes in gene and protein expression during the preferable transition from neurogenesis to gliogenesis may lead us to unravel the erroneous cellular development that occurs in the DS brain.