Involvement of AMP‐activated protein kinase in neuroinflammation and neurodegeneration in the adult and developing brain

International Journal of Developmental Neuroscience - Tập 77 - Trang 48-59 - 2019
Mariko Saito1,2, Mitsuo Saito3, Bhaskar C. Das4
1Division of Neurochemistry, Nathan S. Kline Institute for Psychiatric Research, 140 Old Orangeburg, Orangeburg, NY, 10962, USA
2Department of Psychiatry, New York University Langone Medical Center, 550 First Avenue, New York, NY 10016, USA
3Division of Analytical Psychopharmacology, Nathan S. Kline Institute for Psychiatric Research, 140 Old Orangeburg, Orangeburg, NY, 10962, USA
4Departments of Medicine and Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, Annenberg 19-201, New York, NY, 10029, USA

Tóm tắt

Microglial activation followed by neuroinflammation is a defense mechanism of the brain to eliminate harmful endogenous and exogenous materials including pathogens and damaged tissues, while excessive or chronic neuroinflammation may cause or exacerbate neurodegeneration observed in brain injuries and neurodegenerative diseases. Depending on conditions/environments during activation, microglia acquire distinct phenotypes, such as pro‐inflammatory, anti‐inflammatory, and disease‐associated phenotypes, and show their ability to phagocytose various objects and produce pro‐and anti‐inflammatory mediators. Prevention of excessive inflammation by regulating the microglia's pro/anti‐inflammatory balance is important for alleviating progression of brain injuries and diseases. Among many factors involved in the regulation of microglial phenotypes, cellular energy status plays an important role. Adenosine monophosphate‐activated protein kinase (AMPK), which serves as a master sensor and regulator of energy balance, is considered a candidate molecule. Accumulating evidence from adult rodent studies indicates that AMPK activation promotes anti‐inflammatory responses in microglia exposed to danger signals or various stressors mainly through inhibition of the nuclear factor κB (NF‐κB) signaling and activation of the nuclear factor erythroid‐2‐related factor‐2 (Nrf2) pathway. However, AMPK activation in neurons exposed to stressors/insults may exacerbate neuronal damage if AMPK activation is excessive or prolonged. While AMPK affects microglial activation states and neuronal cell survival rates in both the adult and the developing brain, studies in the developing brain are still scarce, even though activated AMPK is highly expressed especially in the neonatal brain. More in depth studies in the developing brain are important, because neuroinflammation/neurodegeneration occurred during development can result in long‐lasting brain damage.

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International Journal of Developmental Neuroscience

Tập 77

48-59

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