The difference in gliosis induced by β-amyloid and Tau treatments in astrocyte cultures derived from senescence accelerated and normal mouse strains

Abstract

Astrocytes react to various neurodegenerative insults rapidly and undergo changes known as gliosis or astrogliosis. In Alzheimer's disease (AD), a wall of reactive astrocytes surrounds senile plaques of β-amyloid (Aβ) and might play an important role in clearing of Aβ. AD is neuropathologically characterized by the co-existence of two pathological structures, senile plaques and neurofibrillary tangles composed of Aβ and Tau protein respectively. However, the molecular mechanisms underlie astrogliosis and increased expressions of GFAP and other astrogliosis markers are poorly understood. Since AD is age related, the aim of this study is to compare the gliosis of aging prone astrocytes cultured from senescence-accelerated mice and astrocytes from normal mice in response to Aβ and Tau treatment. Our results demonstrated that the aging prone astrocytes have showed larger degree of gliosis than normal astrocytes. Since reactive astrocytes had less ability to support co-cultured neurons as compared with control astrocytes. Therefore, it is likely that aging prone astrocytes might contribute to cell loss or dysfunction associated with insults in AD. In other words, aging prone astrocytes might have decreased ability than normal astrocytes to protect or prevent neuronal dysfunction in AD pathology. In addition, further AD related studies should use aging prone astrocytes instead of normal astrocytes.

Differential Effects of Palmitoylethanolamide against Amyloid-β Induced Toxicity in Cortical Neuronal and Astrocytic Primary Cultures from Wild-Type and 3xTg-AD Mice

“…Finally, there is strong evidence for A␤ 42 -induced impairments in mitochondrial transport, dynamics and function that contribute to synaptic degeneration [47,55,56]. suggests that A␤ 42 causes reactive astrogliosis [64] 586 as previously observed in human AD tissues [64] 587 and in cultured animal astrocytes [29,30,66]. It is cultured astrocytes [29,67,71] along with a consequent increase of intracellular Ca 2+ levels leading to exocytotic glutamate release.…”

Glial dysfunction in the pathogenesis of α-synucleinopathies: emerging concepts

“…Ageing-prone astrocytes, cultured from senescence-accelerated mice, show a larger degree of gliosis than normal astrocytes, after amyloid-β and tau treatment. Besides gliosis, ageing-prone astroglia show a decrease in the ability to support co-cultured neurons, in comparison to normal astroglial cells [134]. Changes in oxidative stress, tau phosphorylation and glutamate uptake of senescence-accelerated murine astrocytes have been observed consistent with reduced neuroprotective capacity in the ageing brain [70].…”

Proteomic study of neuron and astrocyte cultures from senescence‐accelerated mouse SAMP8 reveals degenerative changes

“…Moreover, it is not known the differential involvement of the main brain cell types, neurons and astrocytes. We and others recently demonstrated that SAMP8 cultured astrocytes exhibited age-related disturbances (García-Matas et al 2008;Lü et al 2008Lü et al , 2009) and reduced neuroprotective capacity (García-Matas et al 2008), when compared with SAMR1 astrocytes. Studies on SAMP8 cultured neurons confirmed some agerelated disturbances, such as reduced mitochondrial functionality and higher vulnerability to oxidative injuries (unpublished results).…”