Bibliography for Alzheimer Type II Astrocyte Page:
Bachoo, R. M., Kim, R. S., Ligon, K. L., & et al. (2004). Molecular diversity of astrocytes with implications for neurological disorders. Pnas, 101(21), 8384-8389.
Garman, R. H. (2011). Histology of the central nervous system. Toxicologic Pathology, 39(1), 22-35.
Wren, D. R. and Noble, M. (1989). Oligodendrocytes and oligodendrocyte/type-2 astrocyte progenitor cells of adult rats are specifically susceptible to the lytic effects of complement in absence of antibody. Pnas, 86(22), 9025-9029.
Draft for wiki article additions:
General Background
editAstrocytes belong to a class of glial cells which are known to have specialized functions in the central nervous system. Among many biological roles, astrocytes are important for neuronal development, synaptic transmission, homeostasis, and neuroprotection. For example, astrocytes have many transporters and ion channels that allow for ion balance and static pH levels in order to achieve homeostasis [1]. Although astrocytes are closely related to neurons and neuronal functions, they are not neuronal cells due to their inability to propagate action potentials. However, they are excitable cells that are able to influence synaptic transmission with cellular triggers such as calcium influx [1].
Astrocytes can also respond to CNS injury by undergoing reactive gliosis. This acts as a neuroprotective event by upregulating intermediate filament proteins for structural cellular support. One of these proteins, glial fibrillary acidic protein (GFAP) can be used as a marker for reactive gliosis in damaged tissue [2].
- Alzheimer type II astrocytes are a type of astrocyte that shows specific features from normal astrocytes and are typically seen in pathological cases
Cell Pathology
editWhen hyperammonemia occurs in hepatic encepalopathy, associated phenotypic changes in appearances occur in the cells as well as regulation of gene expression for proteins associated with regulation cell volume and transmission of neuronal impulses [3]. In previous studies of hepatic encepalopathy, the presence of Alzheimer type II astrocytes corresponded to mitochondrial degeneration, as well as previously known phenotypic characteristics such as a prominent nucleolus and enlarged pale nuclei [3]. Additionally, when these astrocytes are exposed to ammonia it causes gliopathy, the dysregulation and dysfunction of the astrocytes [3]. This gliopathy is what is thought to cause encepalopathy in HE [3].
Alzheimer type II astrocytosis occurs when the astrocyte cell is swollen and exhibits a large nucleus along with a significant nucleolus [4]. These cells are typically seen in conditions such as chronic liver disease, where hyperammonemia occurs. This is due to the presence of the enzyme glutamine synthetase, which is able to detoxify ammonia through the amidation of glutamate, producing glutamine in the process [4]. Swelling occurs in these astrocytes due to the increased intracellular glutamine levels which induces osmotic stress on the cell and results in edema (3).
This hypothesis is called the glutamine/osmolyte hypothesis, and has yet to be researched among scientists extensively [5]. However, it is generally thought that ammonia-induced astrocyte swelling can be attributed to oxidative stress that glutamine can exert on the cell, as well as the creation of free radicals that may cause astrocytic damage [5]. It is difficult for researchers to accept that excess intracellular glutamine produced in response to hyperammonemia is the direct cause of astrocytic cell swelling and therefore brain edema, however scientific data is beginning to support the effect that glutamine may have on other chemical reactions that occur in the brain such as the generation of free radicals [5]. This area has not been fully researched yet, and more information about the mechanism by which glutamine creates radicals in the brain and the effect that this has on edema must be elucidated [5].
Alzheimer type II astrocytes can usually be found in diseases where hyperammonemia occurs, such as hepatic encephalopathy [6]. In hepatic encephalopathy, Alzheimer type II astrocytes are characterized by thin chromatin and increased glycogen levels [6]. Although these astrocytes are present in this disease, it has not yet been determined if Alzheimer type II astrocytes are a pathological symptom for HE [6].
- Plan to add more about other conditions where these cells are seen in
- Address that not much research has been done on these specific cells
- Cells have not been determined to cause pathology, only are exhibited in certain cases
References
edit | This is a user sandbox of Gicoo001. You can use it for testing or practicing edits. This is not the sandbox where you should draft your assigned article for a dashboard.wikiedu.org course. To find the right sandbox for your assignment, visit your Dashboard course page and follow the Sandbox Draft link for your assigned article in the My Articles section. |
- ^ a b Sofroniew, Michael V.; Vinters, Harry V. (2009-12-10). "Astrocytes: biology and pathology". Acta Neuropathologica. 119 (1): 7–35. doi:10.1007/s00401-009-0619-8. ISSN 0001-6322.
- ^ Garman, Robert H. "Histology of the central nervous system". Toxicologic Pathology. 39.
- ^ a b c d Ciećko-Michalska, Irena; Szczepanek, Małgorzata; Słowik, Agnieszka; Mach, Tomasz (2012-12-17). "Pathogenesis of Hepatic Encephalopathy". Gastroenterology Research and Practice. 2012: 1–7. doi:10.1155/2012/642108. ISSN 1687-6121. PMC 3534214. PMID 23316223.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b Coltart, Iona; Tranah, Thomas H.; Shawcross, Debbie L. (2013-08-15). "Inflammation and hepatic encephalopathy". Archives of Biochemistry and Biophysics. Hepatic Encephalopathy. 536 (2): 189–196. doi:10.1016/j.abb.2013.03.016.
- ^ a b c d Jayakumar, A. R.; Rao, K. V. Rama; Murthy, Ch. R. K.; Norenberg, M. D. (2006-05-01). "Glutamine in the mechanism of ammonia-induced astrocyte swelling". Neurochemistry International. Glutamate in CNS Metabolism and Neurotransmission: Interactions at the Inter and Intracellular Level. 48 (6–7): 623–628. doi:10.1016/j.neuint.2005.11.017.
- ^ a b c Albrecht, Jan; Jones, E.Anthony. "Hepatic encephalopathy: molecular mechanisms underlying the clinical syndrome". Journal of the Neurological Sciences. 170 (2): 138–146. doi:10.1016/s0022-510x(99)00169-0.