IMR Press / FBL / Volume 13 / Issue 3 / DOI: 10.2741/2751

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


NAD+ and NADH in ischemic brain injury

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1 Department of Neurology, San Francisco Veterans Affairs Medical Center and the University of California at San Francisco, San Francisco, CA

Academic Editor: John Zhang

Front. Biosci. (Landmark Ed) 2008, 13(3), 1141–1151;
Published: 1 January 2008
(This article belongs to the Special Issue New frontiers in neurosurgery research)

NAD+ and NADH have been emerging as the common mediators of energy metabolism, mitochondrial functions, calcium homeostasis, aging and cell death. NAD+ and NADH can affect cell death by various mechanisms, such as influencing energy metabolism, mitochondrial permeability transition pores, and apoptosis-inducing factor. Because energy failure, calcium disregulation and cell death are the key components in the tissue damaging cascade initiated by cerebral ischemia, it is likely that NAD+ and NADH play significant roles in ischemic brain damage. Many studies, including the findings that poly(ADP-ribose) polymerase-1 mediates ischemic brain injury and that NAD+ administration can decrease ischemic brain damage, have suggested significant roles of NAD+ and NADH in the debilitating illness. However, there is still distinct insufficiency of the information regarding the roles of NAD+ and NADH in ischemic brain injury. Because increasing evidence has indicated critical functions of NAD+ and NADH in various biological processes, future studies on the roles of NAD+ and NADH in cerebral ischemia may expose essential mechanisms underlying ischemic brain injury and suggest novel therapeutic strategies for the illness.

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