High affinity hemoglobin and Parkinson's disease.
Identifieur interne : 000629 ( PubMed/Corpus ); précédent : 000628; suivant : 000630High affinity hemoglobin and Parkinson's disease.
Auteurs : Jeffrey Graham ; Douglas Hobson ; Arjuna PonnampalamSource :
- Medical hypotheses [ 1532-2777 ] ; 2014.
English descriptors
- KwdEn :
- MESH :
- chemical , blood : 2,3-Diphosphoglycerate.
- chemical , metabolism : Dopamine, Hemoglobins, Reactive Oxygen Species.
- blood : Parkinson Disease.
- metabolism : Dopaminergic Neurons, Neurons, Substantia Nigra.
- Blood Gas Analysis, Humans, Mutation, Oxidative Stress.
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra (SN) region of the midbrain. Oxidative damage in this region has been shown to play an important role in the pathogenesis of this disease. Human neurons have been discovered to contain hemoglobin, with an increased concentration seen in the neurons of the SN. High affinity hemoglobin is a clinical entity resulting from mutations that create a functional increase in the binding of hemoglobin to oxygen and an inability to efficiently unload it to tissues. This can result in a number of metabolic compensatory changes, including an elevation in circulating hemoglobin and an increase in the molecule 2,3-diphosphoglycerate (2,3-DPG). Population based studies have revealed that patients with PD have elevated hemoglobin as well as 2,3-DPG levels. Based on these observations, we hypothesize that the oxidative damage seen in PD is related to an underlying high affinity hemoglobin subtype.
DOI: 10.1016/j.mehy.2014.10.016
PubMed: 25468785
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pubmed:25468785Le document en format XML
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<author><name sortKey="Graham, Jeffrey" sort="Graham, Jeffrey" uniqKey="Graham J" first="Jeffrey" last="Graham">Jeffrey Graham</name>
<affiliation><nlm:affiliation>Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Hobson, Douglas" sort="Hobson, Douglas" uniqKey="Hobson D" first="Douglas" last="Hobson">Douglas Hobson</name>
<affiliation><nlm:affiliation>Department of Internal Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.</nlm:affiliation>
</affiliation>
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<author><name sortKey="Ponnampalam, Arjuna" sort="Ponnampalam, Arjuna" uniqKey="Ponnampalam A" first="Arjuna" last="Ponnampalam">Arjuna Ponnampalam</name>
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<term>Blood Gas Analysis</term>
<term>Dopamine (metabolism)</term>
<term>Dopaminergic Neurons (metabolism)</term>
<term>Hemoglobins (metabolism)</term>
<term>Humans</term>
<term>Mutation</term>
<term>Neurons (metabolism)</term>
<term>Oxidative Stress</term>
<term>Parkinson Disease (blood)</term>
<term>Reactive Oxygen Species (metabolism)</term>
<term>Substantia Nigra (metabolism)</term>
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<term>Reactive Oxygen Species</term>
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<term>Neurons</term>
<term>Substantia Nigra</term>
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<keywords scheme="MESH" xml:lang="en"><term>Blood Gas Analysis</term>
<term>Humans</term>
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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra (SN) region of the midbrain. Oxidative damage in this region has been shown to play an important role in the pathogenesis of this disease. Human neurons have been discovered to contain hemoglobin, with an increased concentration seen in the neurons of the SN. High affinity hemoglobin is a clinical entity resulting from mutations that create a functional increase in the binding of hemoglobin to oxygen and an inability to efficiently unload it to tissues. This can result in a number of metabolic compensatory changes, including an elevation in circulating hemoglobin and an increase in the molecule 2,3-diphosphoglycerate (2,3-DPG). Population based studies have revealed that patients with PD have elevated hemoglobin as well as 2,3-DPG levels. Based on these observations, we hypothesize that the oxidative damage seen in PD is related to an underlying high affinity hemoglobin subtype.</div>
</front>
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<Abstract><AbstractText>Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra (SN) region of the midbrain. Oxidative damage in this region has been shown to play an important role in the pathogenesis of this disease. Human neurons have been discovered to contain hemoglobin, with an increased concentration seen in the neurons of the SN. High affinity hemoglobin is a clinical entity resulting from mutations that create a functional increase in the binding of hemoglobin to oxygen and an inability to efficiently unload it to tissues. This can result in a number of metabolic compensatory changes, including an elevation in circulating hemoglobin and an increase in the molecule 2,3-diphosphoglycerate (2,3-DPG). Population based studies have revealed that patients with PD have elevated hemoglobin as well as 2,3-DPG levels. Based on these observations, we hypothesize that the oxidative damage seen in PD is related to an underlying high affinity hemoglobin subtype.</AbstractText>
<CopyrightInformation>Copyright © 2014 Elsevier Ltd. All rights reserved.</CopyrightInformation>
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