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Compositions and Methods for Treating Neural Anoxia and Spreading Depression, 2009
Title
Compositions and Methods for Treating Neural Anoxia and Spreading Depression, 2009.
Creator
Dawson-Scully, Ken, Robertson, R. Meldrum, Florida Atlantic University, Armstrong, Gary A.B.
Abstract/Description
Compositions and methods for protecting neural tissue (e.g., neurons) from anoxia and spreading depression (SD) involve inhibiting the cGMP-dependent protein kinase (PKG) pathway. It was discovered that the PKG pathway plays a crucial role in regulating SD and tolerance to anoxia in the central nervous system (CNS). Inhibition of the PKG pathway greatly reduces SD and increases tolerance to anoxia (i.e., hypoxia), while activation of the pathway exacerbates SD pathology. The compositions and...
Show moreCompositions and methods for protecting neural tissue (e.g., neurons) from anoxia and spreading depression (SD) involve inhibiting the cGMP-dependent protein kinase (PKG) pathway. It was discovered that the PKG pathway plays a crucial role in regulating SD and tolerance to anoxia in the central nervous system (CNS). Inhibition of the PKG pathway greatly reduces SD and increases tolerance to anoxia (i.e., hypoxia), while activation of the pathway exacerbates SD pathology. The compositions and methods can be used to treat any condition associated with SD or anoxia, including stroke, spinal cord injury, neurogenerative disease, dizziness, headaches, and migraines.
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Date Issued
2009
PURL
http://purl.flvc.org/fau/fd/FAUIR000255
Format
Document (PDF)
Compositions and Methods for Treating Neural Anoxia and Spreading Depression, 2011
Title
Compositions and Methods for Treating Neural Anoxia and Spreading Depression, 2011.
Creator
Dawson-Scully, Ken, Robertson, R. Meldrum, Florida Atlantic University, Armstrong, Gary A.B.
Abstract/Description
Compositions and methods for protecting neural tissue (e.g., neurons) from anoxia and spreading depression (SD) involve inhibiting the cGMP-dependent protein kinase (PKG) pathway. It was discovered that the PKG pathway plays a crucial role in regulating SD and tolerance to anoxia in the central nervous system (CNS). Inhibition of the PKG pathway greatly reduces SD and increases tolerance to anoxia (i.e., hypoxia), while activation of the pathway exacerbates SD pathology. The compositions and...
Show moreCompositions and methods for protecting neural tissue (e.g., neurons) from anoxia and spreading depression (SD) involve inhibiting the cGMP-dependent protein kinase (PKG) pathway. It was discovered that the PKG pathway plays a crucial role in regulating SD and tolerance to anoxia in the central nervous system (CNS). Inhibition of the PKG pathway greatly reduces SD and increases tolerance to anoxia (i.e., hypoxia), while activation of the pathway exacerbates SD pathology. The compositions and methods can be used to treat any condition associated with SD or anoxia, including stroke, spinal cord injury, neurogenerative disease, dizziness, headaches, and migraines.
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Date Issued
2011
PURL
http://purl.flvc.org/fau/fd/FAUIR000256
Format
Document (PDF)
Glial Hsp70 Protects K+ Homeostasis in the Drosophila Brain during Repetitive Anoxic Depolarization
Title
Glial Hsp70 Protects K+ Homeostasis in the Drosophila Brain during Repetitive Anoxic Depolarization.
Creator
Armstrong, Gary A. B., Xiao, Chengfeng, Krill, Jennifer L., Seroude, Laurent, Dawson-Scully, Ken, Robertson, R. Meldrum, Roman, Gregg
Abstract/Description
Neural tissue is particularly vulnerable to metabolic stress and loss of ion homeostasis. Repetitive stress generally leads to more permanent dysfunction but the mechanisms underlying this progression are poorly understood. We investigated the effects of energetic compromise in Drosophila by targeting the Na+/K+-ATPase. Acute ouabain treatment of intact flies resulted in subsequent repetitive comas that led to death and were associated with transient loss of K+ homeostasis in the brain. Heat...
Show moreNeural tissue is particularly vulnerable to metabolic stress and loss of ion homeostasis. Repetitive stress generally leads to more permanent dysfunction but the mechanisms underlying this progression are poorly understood. We investigated the effects of energetic compromise in Drosophila by targeting the Na+/K+-ATPase. Acute ouabain treatment of intact flies resulted in subsequent repetitive comas that led to death and were associated with transient loss of K+ homeostasis in the brain. Heat shock pre-conditioned flies were resistant to ouabain treatment. To control the timing of repeated loss of ion homeostasis we subjected flies to repetitive anoxia while recording extracellular [K+] in the brain. We show that targeted expression of the chaperone protein Hsp70 in glial cells delays a permanent loss of ion homeostasis associated with repetitive anoxic stress and suggest that this is a useful model for investigating molecular mechanisms of neuroprotection.
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Date Issued
2011-12-12
PURL
http://purl.flvc.org/fau/fd/FAUIR000078
Format
Citation