Abstract

Astrocytes, a class of morphologically and functionally diverse primary homeostatic neuroglia, are key keepers of neural tissue homeostasis and fundamental contributors to brain defence in pathological contexts. Failure of astroglial support and defence facilitate the evolution of neurological diseases, which often results in aberrant synaptic transmission, neurodegeneration and death of neurones. In Alzheimer’s disease (AD), astrocytes undergo complex and multifaceted metamorphoses ranging from atrophy with loss of function to reactive astrogliosis with hypertrophy. Astroglial asthenia underlies reduced homeostatic support and neuroprotection that may account for impaired synaptic transmission and neuronal demise. Reactive astrogliosis which mainly develops in astrocytes associated with senile plaque is prominent at the early to moderate stages of AD manifested by mild cognitive impairment; downregulation of astrogliosis (reflecting astroglial paralysis) is associated with late stages of the disease characterised by severe dementia. Cell-specific therapies aimed at boosting astroglial supportive and defensive capabilities and preventing astroglial paralysis may offer new directions in preventing, arresting, or even curing AD-linked neurodegeneration.

Original languageEnglish
Pages (from-to)1247-1261
Number of pages15
JournalPflugers Archiv European Journal of Physiology
Volume471
Issue number10
Early online date13 Sept 2019
DOIs
Publication statusPublished - 1 Oct 2019

Keywords

  • Alzheimer’s disease
  • Astrocytes
  • Astroglial atrophy
  • Astrogliosis
  • Neurodegeneration
  • Neurological diseases

Research Beacons, Institutes and Platforms

  • Lydia Becker Institute

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