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Hyperammonemia, or high ammonia levels, is a metabolic disturbance characterised by an excess of ammonia in the blood. Severe hyperammonemia is a dangerous condition that may lead to brain injury and death. It may be primary or secondary. Ammonia is a substance that contains nitrogen. It is a product of the catabolism of protein.
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. It's mainly seen in diseases that cause increased levels of ammonia (hyperammonemia), such as chronic liver disease and Wilson's disease. [1]
[2] [6] It may be supported by blood ammonia levels, an electroencephalogram, or computer tomography (CT scan) of the brain. [4] [6] Hepatic encephalopathy is possibly reversible with treatment. [1] This typically involves supportive care and addressing the triggers of the event. [4] Lactulose is frequently used to decrease ammonia levels. [1]
The brain is very complex, and is composed of many different areas and types of tissue, or matter. The different functions of different tissues in the brain may be more or less susceptible to age-induced changes. [6] The brain matter can be broadly classified as either grey matter, or white matter.
The brain has a mechanism to counteract the presence of this waste metabolite. One of the mechanisms involved in the impairment of the brain is the compromise of astrocyte potassium buffering, where astrocytes play a key role. However, as more ammonia crosses, the system gets saturated, leading to astrocyte swelling and brain edema. [10]
The plaques are highly variable in shape and size; in tissue sections immunostained for Aβ, they comprise a log-normal size distribution curve, with an average plaque area of 400-450 square micrometers (μm 2). The smallest plaques (less than 200 μm 2), which often consist of diffuse deposits of Aβ, [4] are particularly numerous. [6]
“The finding that brain tissue from individuals diagnosed with dementia had up to 10 times as much plastic as those without the condition is significant, but it’s important to interpret this ...
The resultant effect of this toxicity can be reduced brain energy metabolism and function. Importantly, the toxic effects of ammonia on astrocyte remodeling can be reduced through administration of L-carnitine. [89] This astrocyte remodeling appears to be mediated through ammonia-induced mitochondrial permeability transition.