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Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with 18F-FDG
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Non-invasive Imaging and Analysis of Cerebral Ischemia in Living Rats Using Positron Emission Tomography with 18F-FDG

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NAD+ and NADH in ischemic brain injury

Weihai Ying1

  • 1Department of Neurology, San Francisco Veterans Affairs Medical Center and the University of California at San Francisco, San Francisco, CA 94121, USA. Weihai.Ying@ucsf.edu

Frontiers in Bioscience : a Journal and Virtual Library
|November 6, 2007
PubMed

Insights

Nicotinamide adenine dinucleotide (NAD+) and its reduced form (NADH) are vital in brain injury. Research suggests these molecules play significant roles in ischemic brain damage, highlighting potential therapeutic targets.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Cell Biology

Background:

  • Nicotinamide adenine dinucleotide (NAD+) and NADH are key mediators of cellular energy metabolism, mitochondrial function, calcium homeostasis, aging, and cell death.
  • These molecules influence cell death pathways, including energy metabolism, mitochondrial permeability transition pores, and apoptosis-inducing factor.
  • Energy failure, calcium dysregulation, and cell death are central to the tissue damage cascade following cerebral ischemia.

Purpose of the Study:

  • To investigate the significant roles of NAD+ and NADH in ischemic brain damage.
  • To explore the potential of NAD+ and NADH as therapeutic targets for cerebral ischemia.

Main Methods:

  • Review of existing studies on NAD+, NADH, and ischemic brain injury.
  • Analysis of mechanisms by which NAD+ and NADH influence cell death and energy metabolism in the context of ischemia.
  • Examination of findings related to poly(ADP-ribose) polymerase-1 and NAD+ administration in ischemic brain injury.

Main Results:

  • Studies indicate that poly(ADP-ribose) polymerase-1 contributes to ischemic brain injury.
  • Administration of NAD+ has been shown to reduce ischemic brain damage.
  • Despite suggestive evidence, a comprehensive understanding of NAD+ and NADH roles in ischemic brain injury remains insufficient.

Conclusions:

  • NAD+ and NADH likely play critical roles in ischemic brain damage due to their involvement in energy metabolism and cell death pathways.
  • Further research into NAD+ and NADH mechanisms in cerebral ischemia is essential.
  • Understanding these roles may reveal underlying mechanisms of ischemic brain injury and identify novel therapeutic strategies.

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