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 Neural Oxidative Metabolism and Death Study Section [NOMD]

The Neural Oxidative Metabolism, Mitochondria and Cell Death [NOMD] Study Section reviews applications studying the molecular mechanisms of neuronal cell death involving aging, neurodegenerative diseases, programmed cell death, necrosis, autophagy, and excitotoxicity; reactive oxygen species and oxidative stress associated with neural injury; and mitochondrial biology of neurons and glia in healthy and diseased states across the life span. Also considered are the roles of genetic factors, trophic molecules and extrinsic influences [including toxins, hormones, and addictive or environmental substances] in these processes, as well as basic aspects of disease, injury, repair and interventional strategies.

Rosters

NOMD Membership Roster               NOMD Meeting Rosters

Topics

  • Functions and mechanisms of action of signaling molecules [such as neurotrophic factors, growth factors, cytokines, glutamate] and electrical activity in regulating cell survival. Intracellular signaling pathways leading to apoptosis, necrosis, autophagy, and excitotoxicity, and their intersection with the signal transduction pathways of survival factors.
  • Oxidative stress; metabolic and energetic demands of neurons and glia; mitochondrial function and localization; mitochondrial dysfunction in disease states including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Amyotrophic Lateral Sclerosis, and stroke.
  • Mechanisms of neuronal cell death due to aging, disease, injury, DNA damage, and environmental or genetic factors. This could include excitotoxins, glutamate, free radicals, metals, and neurodegenerative disease genes, as well as elucidation of excitotoxic, necrotic, autophagic,and apoptotic mechanisms.
  • Studies of mechanisms relevant to the development of neuroprotective or cell survival strategies, such as the administration of exogenous growth factors, or antioxidants, and the use of stem cell therapies.
  • Molecular mechanisms underlying neural injury associated with ischemia, reperfusion injury, traumatic brain injury, hypoxia, hypoglycemia, and excitotoxicity.
  • Gene regulatory mechanisms including shRNA, siRNA, miRNA, and post translational modifications.
  • Animal and cellular models of neurodegenerative disease and injury.

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