Alzheimer type II astrocyte
The Alzheimer type II astrocyte is a pathological type of cell in the brain. Like other astrocytes, it is a non-neuronal glial cell. They are not associated with Alzheimer's disease.
Characteristics
Alzheimer type II astrocytes are visually characterized by an enlarged size and lack of cytoplasm. [1] These astrocytes appear to metabolically hyperactive, and contain vesicular nuclei and basophilic nucleoli. [2] They also contain thin marginal chromatin and excessive amounts of glycogen. [1] Alzheimer type II astrocytes may be found in both cortical and subcortical areas, including the brain stem, cerebellum, cerebral cortex, and thalamus.[3]
Pathology
Alzheimer type II astrocytes are present in hepatic encephalopathy and Wilson's disease.[4] The presence of Alzheimer type astrocytes is a key indicator of hepatic encephalopathy, and may be induced by increased bodily ammonia.[5] The origin of Alzheimer type II astrocytes is unclear, although they are known to arise from astroglial cells in the development of Wilson's disease. [6] Experiments with mice have shown that exposure to manganese leads to the development of Alzheimer's type II astrocytes. [7] This suggests that manganism, a neurological disorder with Parkinson's-like symptoms, is caused by the development of these astrocytes through manganese poisoning.[7]
References
- 1 2 , Albrecht Jan, Jones Anthony E (2000). "Hepatic encephalocity: molecular mechanisms underlying the clinical syndrome." Journal of the Neurological Sciences 172(1): 77.
- ↑ Online Medical Dictionary at CancerWeb
- ↑ , University of Rochester Medical Center. Retrieved 2 December 2015.
- ↑ Blueprints Neurology, 2nd ed.
- ↑ , Norenberg MD (1987). "The role of astrocytes in hepatic encephalopathy." Neurochememical Pathology 6(1-2):13-33.
- ↑ , Bertrand E, et al. (2001). "Neuropathological analysis of pathological forms of astroglia in Wilson's disease." Folia Neuropathologica 39(2):73-79.
- 1 2 , Hazell Alan S, et al. (2006). "Alzheimer type II astrocytic changes following sub-acute exposure to manganese and its prevention by antioxidant treatment." Neuroscience Letters 396(3):167-171.