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La maladie de Parkinson en France (serveur d'exploration)

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Involvement of non-dopaminergic pathways in Parkinson's disease : Pathophysiology and therapeutic implications

Identifieur interne : 000045 ( PascalFrancis/Curation ); précédent : 000044; suivant : 000046

Involvement of non-dopaminergic pathways in Parkinson's disease : Pathophysiology and therapeutic implications

Auteurs : A.-M. Bonnet [France]

Source :

RBID : Pascal:00-0242418

Descripteurs français

English descriptors

Abstract

Parkinson's disease is primarily characterised by degeneration of the nigrostriatal dopaminergic pathways in the basal ganglia. However, non-dopaminergic neurotransmission is also affected in Parkinson's disease. The dysfunction of non-dopaminergic systems explains the principal non-dopaminergic symptoms, such as axial' signs and cognitive impairment. The non-dopaminergic neurotransmitters affected in Parkinson's disease are noradrenaline (norepinephrine), serotonin (5-hydroxytryptamine; 5-HT), glutamate, γ-aminobutyric acid (GABA), acetylcholine and neuropeptides. Dysfunction of these systems can lead to some of the motor symptoms of the disease and may provide targets for pharmacological interventions to treat these symptoms. For example, antagonists of certain glutamate receptors have been found to improve parkinsonian symptoms when given in associated with levodopa, although adverse effects may limit their use. The dysfunction of non-doparninergic neurotransmitter systems in Parkinson's disease is also important because it can lead to non-motor symptoms that are not responsive to dopaminergic therapy and can be a major cause of disability during disease evolution. Dysautonomia is not infrequent in individuals with Parkinson's disease and is characterised by constipation, urinary disorders and orthostatic hypotension, the latter resulting from deficits in adrenergic and noradrenergic neurotransmission. Postural instability is caused by abnormalities in both dopaminergic and non-dopaminergic pathways. Depression is partially a result of dopaminergic denervation, but also of a decrease of serotonergic transmission. Cognitive impairment with frontal lobe-like symptomatology is a result of the dopaminergic deficit but also, at least in part, a cholinergic and noradrenergic deficit. Long term use of levodopa can be associated with complications such as dyskinesias. Although these are treated initially with other dopaminergic treatments, including changes in the levodopa administration schedule and dopamine receptor agonists, there have been attempts to treat dyskinesias with non-dopaminergic drugs. Agents such as glutamate antagonists and opioid antagonists have been found to be useful.
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C01 01    ENG  @0 Parkinson's disease is primarily characterised by degeneration of the nigrostriatal dopaminergic pathways in the basal ganglia. However, non-dopaminergic neurotransmission is also affected in Parkinson's disease. The dysfunction of non-dopaminergic systems explains the principal non-dopaminergic symptoms, such as axial' signs and cognitive impairment. The non-dopaminergic neurotransmitters affected in Parkinson's disease are noradrenaline (norepinephrine), serotonin (5-hydroxytryptamine; 5-HT), glutamate, γ-aminobutyric acid (GABA), acetylcholine and neuropeptides. Dysfunction of these systems can lead to some of the motor symptoms of the disease and may provide targets for pharmacological interventions to treat these symptoms. For example, antagonists of certain glutamate receptors have been found to improve parkinsonian symptoms when given in associated with levodopa, although adverse effects may limit their use. The dysfunction of non-doparninergic neurotransmitter systems in Parkinson's disease is also important because it can lead to non-motor symptoms that are not responsive to dopaminergic therapy and can be a major cause of disability during disease evolution. Dysautonomia is not infrequent in individuals with Parkinson's disease and is characterised by constipation, urinary disorders and orthostatic hypotension, the latter resulting from deficits in adrenergic and noradrenergic neurotransmission. Postural instability is caused by abnormalities in both dopaminergic and non-dopaminergic pathways. Depression is partially a result of dopaminergic denervation, but also of a decrease of serotonergic transmission. Cognitive impairment with frontal lobe-like symptomatology is a result of the dopaminergic deficit but also, at least in part, a cholinergic and noradrenergic deficit. Long term use of levodopa can be associated with complications such as dyskinesias. Although these are treated initially with other dopaminergic treatments, including changes in the levodopa administration schedule and dopamine receptor agonists, there have been attempts to treat dyskinesias with non-dopaminergic drugs. Agents such as glutamate antagonists and opioid antagonists have been found to be useful.
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C07 03  X  ENG  @0 Cerebral disorder @5 39
C07 03  X  SPA  @0 Encéfalo patología @5 39
C07 04  X  FRE  @0 Extrapyramidal syndrome @5 40
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C07 04  X  SPA  @0 Extrapiramidal síndrome @5 40
C07 05  X  FRE  @0 Maladie dégénérative @5 41
C07 05  X  ENG  @0 Degenerative disease @5 41
C07 05  X  SPA  @0 Enfermedad degenerativa @5 41
N21       @1 164

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</fC03>
<fC03 i1="12" i2="X" l="ENG">
<s0>Brain (vertebrata)</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA">
<s0>Encéfalo</s0>
<s5>17</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE">
<s0>Système nerveux central</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG">
<s0>Central nervous system</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA">
<s0>Sistema nervioso central</s0>
<s5>18</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE">
<s0>Neuropeptide</s0>
<s5>19</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG">
<s0>Neuropeptide</s0>
<s5>19</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA">
<s0>Neuropéptido</s0>
<s5>19</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE">
<s0>Catécholamine</s0>
<s5>20</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG">
<s0>Catecholamine</s0>
<s5>20</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA">
<s0>Catecolamina</s0>
<s5>20</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE">
<s0>Sérotonine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>21</s5>
</fC03>
<fC03 i1="16" i2="X" l="ENG">
<s0>Serotonin</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>21</s5>
</fC03>
<fC03 i1="16" i2="X" l="SPA">
<s0>Serotonina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>21</s5>
</fC03>
<fC03 i1="17" i2="X" l="FRE">
<s0>Glutamate</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>22</s5>
</fC03>
<fC03 i1="17" i2="X" l="ENG">
<s0>Glutamate</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>22</s5>
</fC03>
<fC03 i1="17" i2="X" l="SPA">
<s0>Glutamato</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>22</s5>
</fC03>
<fC03 i1="18" i2="X" l="FRE">
<s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>23</s5>
</fC03>
<fC03 i1="18" i2="X" l="ENG">
<s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>23</s5>
</fC03>
<fC03 i1="18" i2="X" l="SPA">
<s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>23</s5>
</fC03>
<fC03 i1="19" i2="X" l="FRE">
<s0>GABA</s0>
<s2>NK</s2>
<s5>24</s5>
</fC03>
<fC03 i1="19" i2="X" l="ENG">
<s0>GABA</s0>
<s2>NK</s2>
<s5>24</s5>
</fC03>
<fC03 i1="19" i2="X" l="SPA">
<s0>GABA</s0>
<s2>NK</s2>
<s5>24</s5>
</fC03>
<fC03 i1="20" i2="X" l="FRE">
<s0>Acétylcholine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>35</s5>
</fC03>
<fC03 i1="20" i2="X" l="ENG">
<s0>Acetylcholine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>35</s5>
</fC03>
<fC03 i1="20" i2="X" l="SPA">
<s0>Acetilcolina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>35</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fN21>
<s1>164</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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