Norepinephrine deficiency in Parkinson's disease: the case for noradrenergic enhancement.
Identifieur interne : 000496 ( Main/Exploration ); précédent : 000495; suivant : 000497Norepinephrine deficiency in Parkinson's disease: the case for noradrenergic enhancement.
Auteurs : Alberto J. Espay [États-Unis] ; Peter A. Lewitt ; Horacio KaufmannSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Autonomic Nervous System Diseases (metabolism), Dopamine (metabolism), Dopamine beta-Hydroxylase (deficiency), Dopamine beta-Hydroxylase (drug effects), Dopamine beta-Hydroxylase (metabolism), Humans, Locus Coeruleus (drug effects), Locus Coeruleus (metabolism), Motor Activity (drug effects), Norepinephrine (deficiency), Norepinephrine (metabolism), Norepinephrine (pharmacology), Parkinson Disease (drug therapy), Parkinson Disease (genetics).
- MESH :
- chemical , deficiency : Dopamine beta-Hydroxylase, Norepinephrine.
- chemical , drug effects : Dopamine beta-Hydroxylase.
- chemical , metabolism : Dopamine, Dopamine beta-Hydroxylase, Norepinephrine.
- drug effects : Locus Coeruleus, Motor Activity.
- drug therapy : Parkinson Disease.
- genetics : Parkinson Disease.
- metabolism : Autonomic Nervous System Diseases, Locus Coeruleus.
- chemical , pharmacology : Norepinephrine.
- Animals, Humans.
Abstract
The dramatic response of most motor and some nonmotor symptoms to dopaminergic therapies has contributed to maintaining the long-established identity of Parkinson's disease (PD) as primarily a nigrostriatal dopamine (DA) deficiency syndrome. However, DA neurotransmission may be neither the first nor the major neurotransmitter casualty in the neurodegenerative sequence of PD. Growing evidence supports earlier norepinephrine (NE) deficiency resulting from selective degeneration of neurons of the locus coeruleus and sympathetic ganglia. Dopaminergic replacement therapy therefore would seem to neglect some of the motor, behavioral, cognitive, and autonomic impairments that are directly or indirectly associated with the marked deficiency of NE in the brain and elsewhere. Therapeutic strategies to enhance NE neurotransmission have undergone only limited pharmacological testing. Currently, these approaches include selective NE reuptake inhibition, presynaptic α2 -adrenergic receptor blockade, and an NE prodrug, the artificial amino acid L-threo-3,4-dihydroxyphenylserine. In addition to reducing the consequences of deficient noradrenergic signaling, enhancement strate gies have the potential for augmenting the effects of dopaminergic therapies in PD. Furthermore, early recognition of the various clinical manifestations associated with NE deficiency, which may precede development of motor symptoms, could provide a window of opportunity for neuroprotective interventions.
DOI: 10.1002/mds.26048
PubMed: 25297066
Affiliations:
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Le document en format XML
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Espay</name><affiliation wicri:level="2"><nlm:affiliation>Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, Ohio, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology, University of Cincinnati, Cincinnati, Ohio</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></affiliation></author><author><name sortKey="Lewitt, Peter A" sort="Lewitt, Peter A" uniqKey="Lewitt P" first="Peter A" last="Lewitt">Peter A. 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However, DA neurotransmission may be neither the first nor the major neurotransmitter casualty in the neurodegenerative sequence of PD. Growing evidence supports earlier norepinephrine (NE) deficiency resulting from selective degeneration of neurons of the locus coeruleus and sympathetic ganglia. Dopaminergic replacement therapy therefore would seem to neglect some of the motor, behavioral, cognitive, and autonomic impairments that are directly or indirectly associated with the marked deficiency of NE in the brain and elsewhere. Therapeutic strategies to enhance NE neurotransmission have undergone only limited pharmacological testing. Currently, these approaches include selective NE reuptake inhibition, presynaptic α2 -adrenergic receptor blockade, and an NE prodrug, the artificial amino acid L-threo-3,4-dihydroxyphenylserine. In addition to reducing the consequences of deficient noradrenergic signaling, enhancement strate gies have the potential for augmenting the effects of dopaminergic therapies in PD. Furthermore, early recognition of the various clinical manifestations associated with NE deficiency, which may precede development of motor symptoms, could provide a window of opportunity for neuroprotective interventions.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Ohio</li></region></list><tree><noCountry><name sortKey="Kaufmann, Horacio" sort="Kaufmann, Horacio" uniqKey="Kaufmann H" first="Horacio" last="Kaufmann">Horacio Kaufmann</name><name sortKey="Lewitt, Peter A" sort="Lewitt, Peter A" uniqKey="Lewitt P" first="Peter A" last="Lewitt">Peter A. Lewitt</name></noCountry><country name="États-Unis"><region name="Ohio"><name sortKey="Espay, Alberto J" sort="Espay, Alberto J" uniqKey="Espay A" first="Alberto J" last="Espay">Alberto J. 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