<unk> s are present in hepatic encephalopathy and Wilson's disease. The presence of<unk> s is a key indicator of hepatic encephalopathy, and may be induced by increased bodily ammonia. In hepatic encephalopathy,<unk> s are characterized by thin chromatin and increased glycogen levels. Although these<unk> s are present in this disease, it has not yet been determined if<unk> s are a pathological symptom for HE. The origin of<unk> s is unclear, although they are known to arise from astroglial cells in the development of Wilson's disease. Experiments with mice have shown that exposure to manganese leads to the development of<unk> 's<unk> <unk><unk> s. This suggests that manganism, a neurological disorder with Parkinson's-like symptoms, is caused by the development of these<unk> s through manganese poisoning. 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. Swelling occurs in these<unk> s due to the increased intracellular glutamine levels which induces osmotic stress on the cell and results in edema. This hypothesis is called the glutamine/osmolyte hypothesis, and has yet to be researched among scientists extensively. However, it is generally thought that ammonia-induced<unk>  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<unk> c damage. It is difficult for researchers to accept that excess intracellular glutamine produced in response to hyperammonemia is the direct cause of<unk> c 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. 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.
Alzheimer type II astrocyte
Anitschkow cell
Pseudounipolar neuron
Koniocellular cell
Dinacharya
Astrogliosis
Neurosphere
Martinotti cell