TY - JOUR
T1 - Reactive astrocytes in Alzheimer's disease
T2 - A double-edged sword
AU - Chun, Heejung
AU - Lee, C. Justin
N1 - Funding Information:
This work was supported by Creative Research Initiative Program , Korean National Research Foundation ( 2015R1A3A2066619 ) and Korea Institute of Science and Technology Institutional Programs (Project No. 2E26860).
Funding Information:
This work was supported by Creative Research Initiative Program, Korean National Research Foundation (2015R1A3A2066619) and Korea Institute of Science and Technology Institutional Programs (Project No. 2E26860).
Publisher Copyright:
© 2017 Elsevier Ireland Ltd and Japan Neuroscience Society
PY - 2018/1
Y1 - 2018/1
N2 - Alzheimer's disease (AD) is a chronic and fatal disease, in which neuronal damage at its late stage cannot be easily reversed. Because AD progression is caused by multiple factors including diverse cellular processes, studies on AD pathogenesis at the molecular and cellular level are challenging. Based on the lessons from unsuccessful neuron-focused research for an AD cure, non-cell autonomous mechanisms including brain inflammation and reactive astrocytes have recently been in the spotlight as potential therapeutic targets for AD. Studies have shown that reactive astrocytes are not only the result of inflammatory defense reactions, but also an active catabolic decomposer that acts by taking up amyloid beta toxins. Here, we give an overview of the characteristics of reactive astrocytes as pathological features of AD. Reactive astrocytes exert biphasic effects, that is, beneficial or detrimental depending on multiple factors. Many efforts have been put forth for defining and characterizing molecular signatures for the beneficial and detrimental reactive astrocytes. In the foreseeable future, manipulating and targeting each established molecular signature should have profound therapeutic implications for the treatment of AD.
AB - Alzheimer's disease (AD) is a chronic and fatal disease, in which neuronal damage at its late stage cannot be easily reversed. Because AD progression is caused by multiple factors including diverse cellular processes, studies on AD pathogenesis at the molecular and cellular level are challenging. Based on the lessons from unsuccessful neuron-focused research for an AD cure, non-cell autonomous mechanisms including brain inflammation and reactive astrocytes have recently been in the spotlight as potential therapeutic targets for AD. Studies have shown that reactive astrocytes are not only the result of inflammatory defense reactions, but also an active catabolic decomposer that acts by taking up amyloid beta toxins. Here, we give an overview of the characteristics of reactive astrocytes as pathological features of AD. Reactive astrocytes exert biphasic effects, that is, beneficial or detrimental depending on multiple factors. Many efforts have been put forth for defining and characterizing molecular signatures for the beneficial and detrimental reactive astrocytes. In the foreseeable future, manipulating and targeting each established molecular signature should have profound therapeutic implications for the treatment of AD.
KW - Alzheimer's disease
KW - Brain inflammation
KW - Reactive astrocytes
UR - http://www.scopus.com/inward/record.url?scp=85037735178&partnerID=8YFLogxK
U2 - 10.1016/j.neures.2017.11.012
DO - 10.1016/j.neures.2017.11.012
M3 - Review article
C2 - 29225140
AN - SCOPUS:85037735178
VL - 126
SP - 44
EP - 52
JO - Neuroscience Research
JF - Neuroscience Research
SN - 0168-0102
ER -