Alzheimer type II astrocyte

The Alzheimer type II astrocyte is thought to be a pathological type of cell in the brain, however its exact pathology remains unknown. Like other astrocytes, it is a non-neuronal glial cell. They are not associated with Alzheimer's disease.

Astrocytes 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. 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. 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.

Alzheimer type II astrocytosis occurs when the astrocyte cell is swollen and exhibits a large nucleus along with a significant nucleolus. Alzheimer type II astrocytes are visually characterized by an enlarged size and lack of cytoplasm. These astrocytes appear to be metabolically hyperactive, and contain vesicular nuclei and basophilic nucleoli. They also contain thin marginal chromatin and excessive amounts of glycogen. Alzheimer type II astrocytes may be found in both cortical and subcortical areas, including the brain stem, cerebellum, cerebral cortex, and thalamus.

When 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. 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. Additionally, when these astrocytes are exposed to ammonia it causes gliopathy, the dysregulation and dysfunction of the astrocytes. This gliopathy is what is thought to cause encephalopathy in HE.

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