TY - CHAP
T1 - Neuroinflammation and oxidative injury in developmental neurotoxicity
AU - Milatovic, Dejan
AU - Zaja-Milatovic, Snjezana
AU - Breyer, Rich M.
AU - Aschner, Michael
AU - Montine, Thomas J.
N1 - Funding Information:
The authors gratefully acknowledge support by grants from the Department of Defense W81XWH-05-1-0239 (DM, MA) and the National Institute of Health (NIH) NS057223 (DM), R01 10563 and 07331 (MA), and ES16754 and AG05136 (TM).
Publisher Copyright:
© 2011 Elsevier Inc. All rights reserved.
PY - 2011/1/1
Y1 - 2011/1/1
N2 - This chapter characterizes the processes of neuroinflammation and related oxidative injury and discusses alterations associated with developmental neurotoxicity. Neuroinflammation is characterized by a host of cellular and molecular changes within the brain. It investigates the effectiveness of drugs currently proposed to inhibit COX, and to suppress innate immune response and/or oxidative damage. The data furnished here imply that α-tocopherol offers broad protection in the cerebrum from oxidative damage. The increased state of neuroinflammation makes the aged brain more vulnerable to the disruptive effects of both intrinsic and extrinsic factors such as disease, infection, toxicants or stress. The exact pattern of cellular and molecular changes depends largely on the type and duration of the inflammatory challenge experienced by the organism. Neuroinflammation can result from classical injuries such as direct insult to the brain that occurs with trauma, encephalitis or ischemia, or from insults such as toxins or infection that follow exposure to bacteria. It is becoming increasingly evident that neuroinflammation and associated oxidative damage play a crucial role in the development and progression of brain diseases. Glia, and in particular microglia, are central to mediating the effects of neuroinflammation.
AB - This chapter characterizes the processes of neuroinflammation and related oxidative injury and discusses alterations associated with developmental neurotoxicity. Neuroinflammation is characterized by a host of cellular and molecular changes within the brain. It investigates the effectiveness of drugs currently proposed to inhibit COX, and to suppress innate immune response and/or oxidative damage. The data furnished here imply that α-tocopherol offers broad protection in the cerebrum from oxidative damage. The increased state of neuroinflammation makes the aged brain more vulnerable to the disruptive effects of both intrinsic and extrinsic factors such as disease, infection, toxicants or stress. The exact pattern of cellular and molecular changes depends largely on the type and duration of the inflammatory challenge experienced by the organism. Neuroinflammation can result from classical injuries such as direct insult to the brain that occurs with trauma, encephalitis or ischemia, or from insults such as toxins or infection that follow exposure to bacteria. It is becoming increasingly evident that neuroinflammation and associated oxidative damage play a crucial role in the development and progression of brain diseases. Glia, and in particular microglia, are central to mediating the effects of neuroinflammation.
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U2 - 10.1016/B978-0-12-382032-7.10064-5
DO - 10.1016/B978-0-12-382032-7.10064-5
M3 - Chapter
AN - SCOPUS:84884466706
SP - 847
EP - 854
BT - Reproductive and Developmental Toxicology
PB - Elsevier
ER -