Astrocytes: Consequences for Neuroinflammatory Pathogenesis of Alzheimer’s Disease

Alzheimer’s disease (AD) is a neurodegenerative disease with main clinical signs of dementia and cognitive impairment. Neuroinflammation is involved in the onset of numerous neurodegenerative disorders. Astrocyte is the most common kind of glial cells in the central nervous system (CNS) and seems to be involved in the induction of neuroinflammation. Traumatic conditions make astrocytes to overexpressedproinflammatory chemokines and cytokines, which are related to the pathogenesis of AD. Cytokines and associated molecules have significant roles in both neuroprotection and neurodegeneration in the CNS. During early AD pathogenesis, amyloid beta (Aβ),S100B and IL1-β could take about a vicious cycle of Aβ generation between astrocytes and neurons that is leading to progressive and chronic neuroinflammation. In progressive stages of AD, TRAIL secreted from astrocytes have been revealed to bind to death receptor 5 (DR5) on neurons to activate apoptosis in a caspase-8- dependent way. Also, astrocytes could be reactivated by TGFβ1 to make more Aβ and to undergo the aggravating astrogliosis. TGFβ2 was also detected to cooperate with Aβ to make neuronal demise. Conclusion: According to the above expressions, it is probable that treatments effective at neuroprotection also improve astrocyte-neuron interactions. Though, this possibility has not been completely studied. Astrocytes secreting chemokines and cytokines in the early stage of AD make a novel potential therapeutic target and suggestion the possibility of developing novel medications to cure AD by intervening neuroinflammation