DNA Synthesis in Alzheimer Type II Astrocytosis

Ammonia Affects Astroglial Proliferation in Culture

“…The first studies on the effect of ammonia in in vivo models suggested there to be an increase in astroglial proliferation [ 9 , 10 ]. In fact, DNA synthesis has been shown in Alzheimer type II astrocytes, a cell type that appears in HE [ 19 ]. However, the results of the present work show that ammonia reduces the proliferative activity of astroglial cells in culture.…”

“…Neither BrdU incorporation nor mitotic figures were observed in the liver of rats in an in vivo model of fulminant hepatic failure associated with hyperammonemia [ 28 ]. However, DNA synthesis and mitotic divisions have been described in Alzheimer type II astrocytes, cells associated with HE [ 19 ]. To determine whether the inhibition of DNA synthesis was due to an effect of ammonia and/or glutamine on DNA polymerase, the functioning of this enzyme under high ammonia concentrations was tested using PCR.…”

Ammonia Affects Astroglial Proliferation in Culture

“…The first studies on the effect of ammonia in in vivo models suggested there to be an increase in astroglial proliferation [ 9 , 10 ]. In fact, DNA synthesis has been shown in Alzheimer type II astrocytes, a cell type that appears in HE [ 19 ]. However, the results of the present work show that ammonia reduces the proliferative activity of astroglial cells in culture.…”

“…Neither BrdU incorporation nor mitotic figures were observed in the liver of rats in an in vivo model of fulminant hepatic failure associated with hyperammonemia [ 28 ]. However, DNA synthesis and mitotic divisions have been described in Alzheimer type II astrocytes, cells associated with HE [ 19 ]. To determine whether the inhibition of DNA synthesis was due to an effect of ammonia and/or glutamine on DNA polymerase, the functioning of this enzyme under high ammonia concentrations was tested using PCR.…”

Microglial proliferation in the brain of chronic alcoholics with hepatic encephalopathy

“…The proliferative capacity of the glial cells in the human brain has not been as widely studied despite primary glial diseases such as HE and multiple sclerosis potentially benefitting from restorative therapies. In 1989, Brumback and Lapham demonstrated very rare astrocytic proliferation in the human brain, however there have been no further studies confirming their findings (Brumback and Lapham 1989). It has been suggested that oligodendrocytes may be replaced in pathological conditions such as epilepsy by their precursor, oligodendrocyte progenitor cells, although the quantity of these cells and even their existence in the normal human brain remains an area of ongoing debate (Chang et al 2000; Geha et al 2010; Rhee et al 2009).…”

Motor performance as a predictor of blood levels of ammonia and inflammatory biomarkers in patients with liver cirrhosis

“…Due to liver failure, other organs take on roles in the transformation of ammonia into glutamine, such as skeletal muscle, kidneys and brain [ 19 ]. In the brain, astrocytes undergo a series of morphological changes compatible with Alzheimer’s disease [ 20 , 21 ], and subsequent elevation of intracellular glutamine. This generates osmotic stress that causes astrocytes to swell [ 22 ], dysregulation of metabolic pathways in astrocytes, oxidative stress, and cerebral edema [ 23 ].…”

Ammonia Affects Astroglial Proliferation in Culture

“…The first studies on the effect of ammonia in in vivo models suggested there to be an increase in astroglial proliferation [ 9 , 10 ]. In fact, DNA synthesis has been shown in Alzheimer type II astrocytes, a cell type that appears in HE [ 19 ]. However, the results of the present work show that ammonia reduces the proliferative activity of astroglial cells in culture.…”

“…Neither BrdU incorporation nor mitotic figures were observed in the liver of rats in an in vivo model of fulminant hepatic failure associated with hyperammonemia [ 28 ]. However, DNA synthesis and mitotic divisions have been described in Alzheimer type II astrocytes, cells associated with HE [ 19 ]. To determine whether the inhibition of DNA synthesis was due to an effect of ammonia and/or glutamine on DNA polymerase, the functioning of this enzyme under high ammonia concentrations was tested using PCR.…”

Microglial proliferation in the brain of chronic alcoholics with hepatic encephalopathy

“…The proliferative capacity of the glial cells in the human brain has not been as widely studied despite primary glial diseases such as HE and multiple sclerosis potentially benefitting from restorative therapies. In 1989, Brumback and Lapham demonstrated very rare astrocytic proliferation in the human brain, however there have been no further studies confirming their findings (Brumback and Lapham 1989). It has been suggested that oligodendrocytes may be replaced in pathological conditions such as epilepsy by their precursor, oligodendrocyte progenitor cells, although the quantity of these cells and even their existence in the normal human brain remains an area of ongoing debate (Chang et al 2000; Geha et al 2010; Rhee et al 2009).…”

Motor performance as a predictor of blood levels of ammonia and inflammatory biomarkers in patients with liver cirrhosis

“…Due to liver failure, other organs take on roles in the transformation of ammonia into glutamine, such as skeletal muscle, kidneys and brain [ 19 ]. In the brain, astrocytes undergo a series of morphological changes compatible with Alzheimer’s disease [ 20 , 21 ], and subsequent elevation of intracellular glutamine. This generates osmotic stress that causes astrocytes to swell [ 22 ], dysregulation of metabolic pathways in astrocytes, oxidative stress, and cerebral edema [ 23 ].…”

Ammonia Affects Astroglial Proliferation in Culture

“…The first studies on the effect of ammonia in in vivo models suggested there to be an increase in astroglial proliferation [ 9 , 10 ]. In fact, DNA synthesis has been shown in Alzheimer type II astrocytes, a cell type that appears in HE [ 19 ]. However, the results of the present work show that ammonia reduces the proliferative activity of astroglial cells in culture.…”

“…Neither BrdU incorporation nor mitotic figures were observed in the liver of rats in an in vivo model of fulminant hepatic failure associated with hyperammonemia [ 28 ]. However, DNA synthesis and mitotic divisions have been described in Alzheimer type II astrocytes, cells associated with HE [ 19 ]. To determine whether the inhibition of DNA synthesis was due to an effect of ammonia and/or glutamine on DNA polymerase, the functioning of this enzyme under high ammonia concentrations was tested using PCR.…”

Microglial proliferation in the brain of chronic alcoholics with hepatic encephalopathy

“…The proliferative capacity of the glial cells in the human brain has not been as widely studied despite primary glial diseases such as HE and multiple sclerosis potentially benefitting from restorative therapies. In 1989, Brumback and Lapham demonstrated very rare astrocytic proliferation in the human brain, however there have been no further studies confirming their findings (Brumback and Lapham 1989). It has been suggested that oligodendrocytes may be replaced in pathological conditions such as epilepsy by their precursor, oligodendrocyte progenitor cells, although the quantity of these cells and even their existence in the normal human brain remains an area of ongoing debate (Chang et al 2000; Geha et al 2010; Rhee et al 2009).…”

Motor performance as a predictor of blood levels of ammonia and inflammatory biomarkers in patients with liver cirrhosis

“…Due to liver failure, other organs take on roles in the transformation of ammonia into glutamine, such as skeletal muscle, kidneys and brain [ 19 ]. In the brain, astrocytes undergo a series of morphological changes compatible with Alzheimer’s disease [ 20 , 21 ], and subsequent elevation of intracellular glutamine. This generates osmotic stress that causes astrocytes to swell [ 22 ], dysregulation of metabolic pathways in astrocytes, oxidative stress, and cerebral edema [ 23 ].…”