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Getting to NO Alzheimer's disease: neuroprotection versus neurotoxicity mediated by nitric oxide

Journal Article


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Abstract


  • Alzheimer's disease (AD) is a neurodegenerative disorder involving the loss of neurons in the brain which leads to progressive memory loss and behavioral changes. To date, there are only limited medications for AD and no known cure. Nitric oxide (NO) has long been considered part of the neurotoxic insult caused by neuroinflammation in the Alzheimer's brain. However, focusing on early developments, prior to the appearance of cognitive symptoms, is changing that perception. This has highlighted a compensatory, neuroprotective role for NO that protects synapses by increasing neuronal excitability. A potential mechanism for augmentation of excitability by NO is via modulation of voltage-gated potassium channel activity (Kv7 and Kv2). Identification of the ionic mechanisms and signaling pathways that mediate this protection is an important next step for the field. Harnessing the protective role of NO and related signaling pathways could provide a therapeutic avenue that prevents synapse loss early in disease.

Authors


Publication Date


  • 2016

Citation


  • Balez, R. & Ooi, L. (2016). Getting to NO Alzheimer's disease: neuroprotection versus neurotoxicity mediated by nitric oxide. Oxidativ Medicine and Cellular Longevity, 2016 3806157.

Scopus Eid


  • 2-s2.0-84949969049

Ro Full-text Url


  • http://ro.uow.edu.au/cgi/viewcontent.cgi?article=4992&context=smhpapers

Ro Metadata Url


  • http://ro.uow.edu.au/smhpapers/3968

Has Global Citation Frequency


Start Page


  • 3806157

Volume


  • 2016

Place Of Publication


  • United States

Abstract


  • Alzheimer's disease (AD) is a neurodegenerative disorder involving the loss of neurons in the brain which leads to progressive memory loss and behavioral changes. To date, there are only limited medications for AD and no known cure. Nitric oxide (NO) has long been considered part of the neurotoxic insult caused by neuroinflammation in the Alzheimer's brain. However, focusing on early developments, prior to the appearance of cognitive symptoms, is changing that perception. This has highlighted a compensatory, neuroprotective role for NO that protects synapses by increasing neuronal excitability. A potential mechanism for augmentation of excitability by NO is via modulation of voltage-gated potassium channel activity (Kv7 and Kv2). Identification of the ionic mechanisms and signaling pathways that mediate this protection is an important next step for the field. Harnessing the protective role of NO and related signaling pathways could provide a therapeutic avenue that prevents synapse loss early in disease.

Authors


Publication Date


  • 2016

Citation


  • Balez, R. & Ooi, L. (2016). Getting to NO Alzheimer's disease: neuroprotection versus neurotoxicity mediated by nitric oxide. Oxidativ Medicine and Cellular Longevity, 2016 3806157.

Scopus Eid


  • 2-s2.0-84949969049

Ro Full-text Url


  • http://ro.uow.edu.au/cgi/viewcontent.cgi?article=4992&context=smhpapers

Ro Metadata Url


  • http://ro.uow.edu.au/smhpapers/3968

Has Global Citation Frequency


Start Page


  • 3806157

Volume


  • 2016

Place Of Publication


  • United States