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Phytotherapeutic Potential For the Treatment of Alzheimer’s Disease
Published in Atanu Bhattacharjee, Akula Ramakrishna, Magisetty Obulesu, Phytomedicine and Alzheimer’s Disease, 2020
Muhammad Akram, Atanu Bhattacharjee, Naveed Munir, Naheed Akhter, Fozia Anjum, Abida Parveen, Samreen Gul Khan, Muhammad Daniyal, Muhammad Riaz, Fahad Said Khan, Rumaisa Ansari, Umme Laila
Apolipoprotein E is also a causative agent in the development of AD. Different form of apolipoprotein E are present, like apolipoproteins E2, 3, and 4. Glial cells of the brain, which are also called astrocytes, produce these proteins. The risk of developing AD is greater in the presence of higher apolipoprotein E4 concentrations (Aaronson, Van Den Eeden et al. 2017). If the level of this protein increases, then the probability of death is also increased (Harris, Brecht et al. 2003). AD is also associated with E693G mutations in a gene encoding an amyloid precursor protein (Nilsberth, Westlind-Danielsson et al. 2001). Furthermore, AD is caused by oxidative stress because, in this situation, demand by the brain for oxygen is increased (Butterfield and Lauderback 2002). AD is also associated with some pathogens like Chlamydia pneumoniae, which enter the brain tissue and damage brain cells (Harris, Brecht et al. 2003). AD is more common in females, smokers, obese people, patients with high blood pressure or a high level of cholesterol, whereas previous trauma, changes in sleep pattern, and Down syndrome can all increase the risk of AD (Simonson 2018).
Many Applications of Hemp in Neurological & Gut-Brain Axis *
Published in Betty Wedman-St Louis, Cannabis as Medicine, 2019
In the neurons of healthy brains, there is a lower expression of CB2 receptors. However, a significant increase in expression of these receptors is noted in reactive microglia and activated astrocytes during neuroinflammation.5,6 Microglia are cells in the brain and spinal cord. When they become reactive, it is associated with neurodegenerative diseases. Activated microglia modulate inflammatory responses to pathogens and injury by signaling the synthesis of pro-inflammatory cytokines. Similarly, diseases that impact the central nervous system activate astrocytes. The fact that CB2 receptors are highly expressed when both these types of cells are activated may indicate they are needed to combat inflammation. This led researchers to conclude, “Therefore, the CB2 receptors have the potential to restrain the inflammatory processes that contribute to the declines in neural function occurring in a number of neurodegenerative disorders.”2
Nervous System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Mark T. Butt, Alys Bradley, Robert Sills
In addition to their role in supporting endothelial cells forming the BBB, astrocytes respond to a variety of stimuli in the central component of the nervous system. Astrocytes may form the so-called glial scars in areas of small tissue loss but tend to form a wall of cells around larger areas of cavitation (Norenberg 2005). Astrocytes become reactive (enlarged and more numerous) in response to neuronal injury, degenerative conditions, chronic edema, axonal degeneration, and a wide variety of other changes in the brain and spinal cord. As such, staining for astrocytes, generally using an immunohistochemical stain for glial fibrillary acidic protein (GFAP), an intermediate filament expressed most prominently in astrocytes, is an excellent adjunct to traditional H&E stains when examining the brain and spinal cord. Enlarged/reactive astrocytes can also be detected with H&E staining but not with the sensitivity and specificity provided by the GFAP stain. Astrocytes are the most common cells in the brain and contain numerous receptors for neurotransmitters (Agulhon et al. 2008). Astrocyte processes are in contact with most neuronal structures (cell body, axon, dendrite) and form the glial limitans, a continuous layer of astrocyte foot processes that cover the brain and spinal cord, and continue into the superficial aspects of the perivascular space surrounding blood vessels entering the meningeal surface of the brain/cord.
An overview: CRISPR/Cas-based gene editing for viral vaccine development
Published in Expert Review of Vaccines, 2022
Santosh Bhujbal, Rushikesh Bhujbal, Prabhanjan Giram
Christine Kunze et al. explored how astrocytes, the most prevalent cells in the brain, play a role in a variety of neurodegenerative diseases. They found that HIV-1 can survive in astrocytes, producing an increase in HIV load and neurological complications in infected people. They used a synthetic surface peptide to design a new Adeno-associated virus-based vector (AAV9P1) for astrocyte transduction. They next looked at the prospect of using AAV9P1 vectors to deliver HIV-inhibitory genes to astrocytes by creating AAV9P1 vectors that included CRISPR/Cas9 HIV-1 pro-viral editing genes. When compared to un-transduced cells, vessels with these vectors showed significantly lower provirus reactivation. They also discovered that AAV9P1 could be used to transfer genes to astrocytes and could also help inactivate or destroy HIV-1 proviruses stored in astrocytes [151].
Circumventing the packaging limit of AAV-mediated gene replacement therapy for neurological disorders
Published in Expert Opinion on Biological Therapy, 2022
Lara Marrone, Paolo M. Marchi, Mimoun Azzouz
The nervous system is a network of specialized cells involved in signal acquisition, processing and transmission. Structurally, it is classified into two components: (i) the central nervous system (CNS), comprising the brain, spinal cord, and retina; (ii) the peripheral nervous system (PNS), consisting of nerves (cranial, spinal and peripheral) connecting the CNS to the rest of the body as well as to the surrounding environment. Importantly, other cell types than neurons play a critical role in maintaining the architecture and homeostasis of the nervous system. These cells, collectively referred to as glia (from the Greek ‘glue’), support, protect and/or nourish neurons [74]. Particularly, oligodendrocytes and Schwann cells generate the myelin sheath that insulates nerve axons enabling impulse conduction [75]. The microglia, a population of CNS-resident macrophages, patrols the CNS actively releasing signalling molecules involved in the crosstalk among the different cell populations composing the brain [76]. Finally, astrocytes provide axon guidance and synaptic support via the uptake, recycling and release of neurotransmitters; they additionally preserve osmolarity, protect neurons from oxidative stress, and participate in the formation and regulation of the BBB [77].
Blood-based traumatic brain injury biomarkers – Clinical utilities and regulatory pathways in the United States, Europe and Canada
Published in Expert Review of Molecular Diagnostics, 2021
Kevin K. Wang, Jennifer C. Munoz Pareja, Stefania Mondello, Ramon Diaz-Arrastia, Cheryl Wellington, Kimbra Kenney, Ava M. Puccio, Jamie Hutchison, Nicole McKinnon, David O. Okonkwo, Zhihui Yang, Firas Kobeissy, J. Adrian Tyndall, András Büki, Endre Czeiter, Maria C. Pareja Zabala, Nithya Gandham, Rebecca Berman
In healthy brains, astrocytes play essential roles in supporting neurons, modulating neuronal functions, and serving as the interface between the neuro-vasculature and neuronal activities. The most commonly studied astroglial TBI biofluid-biomarker is S100B. Elevated circulating S100B concentrations are associated with secondary injury progression and poor prognosis [23,34,35]. In 2013, the Scandinavian Neurotrauma Committee published evidence-based guidelines for the initial management of TBI in adults and incorporated S100B into the diagnosis of TBI-associated CT abnormalities to reduce unnecessary CT scans and undue radiation exposure in a subset of patients [36]. S100B has also been proposed to be a sensitive marker for blood–brain barrier (BBB) permeability but lacks specificity due to extracranial sources, such as Langerhan’s cells, adipocytes, epithelial cells, cardiac and skeletal muscle cells, and chondrocytes [37,38]. Moreover, reference ranges significantly differ when comparing children to adult populations and should be taken into consideration [39–42]. The clinical characterization of blood levels of S100B for moderate/severe and for mild TBI are now outlined in Suppl. Table 1.