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Prospects of Nanotechnology in Brain Targeting Drug Delivery
Published in Bhaskar Mazumder, Subhabrata Ray, Paulami Pal, Yashwant Pathak, Nanotechnology, 2019
Srijita Chakrabarti, Probin Kr Roy, Pronobesh Chattopadhyay, Bhaskar Mazumder
The macroglia is comprised of oligodendrocytes and astrocytes, which, like neurons, possess ectodermal origins and proliferate throughout life, particularly triggered by an injury (Peters et al., 1991). Astrocytes have a star-shaped morphology and are comprised of numerous cytoplasmic fibrils of which the glial acidic fibrillary protein is the chief component (Walz, 2000). Astrocytes form the structural framework for the neurons and control their biochemical environment. Astrocytes are nonexcitable cells with a large membrane potential, which is sensitive to extracellular potassium ion (K+) concentration changes (Kuffler et al., 1966). Astrocytes play an active role in the homeostatic maintenance of the CNS by locally removing excess K+ which has been released from active neurons. Astrocytes are also involved in the initiation and regulation of immune and inflammatory events during injury and infection. They can inactivate neurotransmitters and regulate and produce growth factors and cytokines. Many of these astrocytes are involved in the production of apolipoprotein E (ApoE) (Lee et al., 2001). The function of the BBB is dynamically regulated by various cells, including astrocytes, neurons, and pericytes.
Tissue Structure and Function
Published in Joseph W. Freeman, Debabrata Banerjee, Building Tissues, 2018
Joseph W. Freeman, Debabrata Banerjee
Astrocytes are star-shaped neuroglia that are present in the spinal cord and brain (CNS). They supply nutrients to neurons, physically support neurons, repair damaged nervous tissue, bind neurons to capillaries, and maintain the blood-brain barrier (Figure 4.26). Astrocytes facilitate some communication between neurons by wrapping around neural synapses and through the release of neurotransmitters such as glutamate. Ependymal cells are ciliated neuroglia that are found within the walls of ventricles (cavities) in the brain and in the spinal cord (Figure 4.27). In the ventricles, the ependymal cells secrete cerebrospinal fluid (CSF), which surrounds the brain protecting it from physical injury and removing toxins from around the brain, depositing them into the bloodstream.
Electrosmog from Communication Equipment
Published in William J. Rea, EMF Effects from Power Sources and Electrosmog, 2018
Glial cells support neurons, release growth factors, and remove debris after injury or neuronal death. Astrocytes help form the blood–brain barrier that prevents toxic substances circulating in the blood from entering the brain. It was proposed many years ago that overexpression of GFAP is the response of astrocytes when oxidative stress occurs,129 which is being reported to take place in brain tissues after exposure of guinea pigs to mobile phone radiation.130 Since GFAP is a sensitive biomarker for neurotoxicity, these findings may indicate neuronal tissue injury caused by EMR or probable injury to the blood–brain barrier, reported to be an effect of exposure.131,132 Immunoblotting with anti-GFAP confirmed the proteomics data in general.
The effect of experimentally-induced diabetes on rat hippocampus and the potential neuroprotective effect of Cerebrolysin combined with insulin. A histological and immunohistochemical study
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Doaa El-Adli, Salwa A. Gawish, Amany AbdElFattah Mohamed AbdElFattah, Mona Fm. Soliman
In addition to mitochondrial changes and expression of caspase-3 and caspase-8 as previously explained [37], diabetic immunohistochemical changes can be correlated to dysregulation of PI3K-Akt (phosphoinositide 3-kinase/protein kinase B) signaling pathway and to increased expression of transcription factor NF-kB (nuclear factor kappa B). STZ reduces the phosphorylated form of AKT, increases the expression of iNOS (inducible nitric oxide synthase) & Nf-kB and decreases pGSK-3β (Glycogen synthase kinase-3 beta) level, leading to apoptosis [19]. TNF-α activity is related to activation of two transcription factors; NF-kB and activating protein-1. Both mediate transcription of pro-inflammatory cytokines [43]. Mammalian target of rapamycin (mTOR) is an essential molecule in the PI3K/AKT and NF-κB signaling pathway. mTOR is increased by hyperglycemia and activates NF-κB leading to synaptic dysfunction [44,45]. Overexpression of GFAP is due to astrogliosis. Astrocytes can perform anti-oxidant function, produce neuroprotective & pro-inflammatory agents and protect the surrounding healthy tissue from the spread of injury and inflammatory cells [46].
Astrocyte 3D culture and bioprinting using peptide functionalized hyaluronan hydrogels
Published in Science and Technology of Advanced Materials, 2023
Isabelle Matthiesen, Michael Jury, Fatemeh Rasti Boroojeni, Saskia L. Ludwig, Muriel Holzreuter, Sebastian Buchmann, Andrea Åman Träger, Robert Selegård, Thomas E. Winkler, Daniel Aili, Anna Herland
Of all the cells that make up the human brain, astrocytes are the most abundant cell type. Astrocytes are involved in synapse formation and function, as well as metabolic activities to support neurons through glutamate clearance at the synaptic cleft [1–3]. Astrocytes also constitute a key role in the formation of the gliovascular unit, where they interact with brain endothelial cells, pericytes, and vascular smooth muscle cells as well as extracellular matrix (ECM) components to form the blood–brain barrier (BBB). The BBB regulates the homeostasis of the central nervous system by controlling transport and exchange of molecules between the blood and the brain [4]. In addition to cell–cell interactions, astrocytes interact extensively with the ECM and the gliovascular basal lamina components of the BBB [5]. The basal lamina is rich in laminins and primarily interacts with the astrocytic endfeet [6]. The interactions between astrocytes and the ECM are also thought to influence the astrocytic response to injury, inflammation, and disease [7].
Neuroprotective role of herbal alternatives in circumventing Alzheimer’s disease through multi-targeting approach - a review
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Sunil K Ravi, Balenahalli Narasingappa Ramesh, Shilpa Kj, Jagadesha Poyya, Jyothsna Karanth, N.G Raju, Chandrashekhar G Joshi
The formation of NFTs and senile plaques are the main histopathological hallmarks of AD [11]. The senile plaques contain amyloid-beta (Aβ) peptide, which consists of 37–49 amino acid residues and are formed by the extracellular and transmembrane domains of amyloid precursor protein (APP) [12]. In plaques, the oligomers might be trapped in fibrillar aggregates. Oligomers may be the hazardous Aβ species that contribute to signaling pathway deregulation (Fyn, FAK, GSK3b, and CDK5), causing changes in cytoskeletal and synaptic proteins, as well as synaptic and neural damage [13] (Figure 1). During sporadic AD, APP is cleaved by gamma and beta secretases to form 4 kDa Aβ peptide. The cleavage product has a strong tendency to form aggregates. Aβ accumulation has been one of the major pathological events resulting from an imbalance between production and clearance [14]. The Aβ aggregation process initiates by self-assembling of Aβ monomers into low molecular weight oligomers, which in turn results in the formation of high molecular weight oligomers known as soluble aggregation intermediates. These further aggregate to form fibrils and accumulate in the brain [15,16]. It is believed that microglia and astrocytes then mount an inflammatory response to clear the amyloid aggregates, and this inflammation likely causes the destruction of adjacent neurons and their neurites.