Research Article

Biogerontology

, Volume 10, Issue 6, pp 695-710

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

  • Lanhai LüAffiliated withDepartment of Anatomy, School of Medicine, Sun Yat-sen University
  • , Ying T. MakAffiliated withDepartment of Anatomy, Chinese University of Hong Kong
  • , Marong FangAffiliated withInstitute of Cell Biology, Medical College of Zhejiang University
  • , David T. YewAffiliated withDepartment of Anatomy, Chinese University of Hong Kong Email author 

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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.

Keywords

Astrogliosis Alzheimer’s disease Aging prone Astrocyte Neurodegenerative insult