MovDisordV3, PascalFrancis, Curation, bibRecord, 001756

Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy

Identifieur interne : 001756 ( PascalFrancis/Curation ); précédent : 001755; suivant : 001757

Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy

Auteurs : Naomi M. Warren [Royaume-Uni] ; Margaret A. Piggott [Royaume-Uni] ; Elizabeth Greally [Royaume-Uni] ; Michelle Lake [Royaume-Uni] ; Andrew J. Lees [Royaume-Uni] ; David J. Burn [Royaume-Uni]

Source :

Movement disorders [ 0885-3185 ] ; 2007.

RBID : Pascal:07-0448795

Descripteurs français

Pascal (Inist)
- Système nerveux pathologie, Noyau gris central.

English descriptors

KwdEn :
- Basal ganglion, Nervous system diseases.

Abstract

Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder. In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, ¹²⁵I PE2I and dopamine D2 receptors, ¹²⁵I epidepride) and cholinergic (nicotinic α4β2 receptors, ¹²⁵I 5IA85380 and muscarinic Ml receptors, ³H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic Ml receptors were unchanged compared with controls. These results do not account for the poor response to dopaminergic and cholinergic replacement therapies in PSP, and suggest relative preservation of postsynaptic striatal projection neurones bearing D2/M1 receptors.

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A11	`01`	`1`		`@1 WARREN (Naomi M.)`
A11	`02`	`1`		`@1 PIGGOTT (Margaret A.)`
A11	`03`	`1`		`@1 GREALLY (Elizabeth)`
A11	`04`	`1`		`@1 LAKE (Michelle)`
A11	`05`	`1`		`@1 LEES (Andrew J.)`
A11	`06`	`1`		`@1 BURN (David J.)`
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C01	`01`		`ENG`	@0 Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder. In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, ¹²⁵I PE2I and dopamine D2 receptors, ¹²⁵I epidepride) and cholinergic (nicotinic α4β2 receptors, ¹²⁵I 5IA85380 and muscarinic Ml receptors, ³H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic Ml receptors were unchanged compared with controls. These results do not account for the poor response to dopaminergic and cholinergic replacement therapies in PSP, and suggest relative preservation of postsynaptic striatal projection neurones bearing D2/M1 receptors.
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C03	`02`	`X`	`FRE`	`@0 Noyau gris central @5 09`
C03	`02`	`X`	`ENG`	`@0 Basal ganglion @5 09`
C03	`02`	`X`	`SPA`	`@0 Núcleo basal @5 09`
C07	`01`	`X`	`FRE`	`@0 Encéphale @5 37`
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C07	`02`	`X`	`SPA`	`@0 Sistema nervioso central @5 38`
N21				`@1 295`
N44	`01`			`@1 OTO`
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<front><div type="abstract" xml:lang="en">Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder. In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, <sup>125</sup>
I PE2I and dopamine D2 receptors, <sup>125</sup>
I epidepride) and cholinergic (nicotinic α4β2 receptors, <sup>125</sup>
I 5IA85380 and muscarinic Ml receptors, <sup>3</sup>
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<fC01 i1="01" l="ENG"><s0>Progressive Supranuclear Palsy (PSP) is a progressive neurodegenerative disorder. In contrast to Parkinson's disease (PD) and dementia with Lewy bodies (DLB), replacement therapy with dopaminergic and cholinergic agents in PSP has been disappointing. The neurochemical basis for this is unclear. Our objective was to measure dopaminergic and cholinergic receptors in the basal ganglia of PSP and control brains. We measured, autoradiographically, dopaminergic (dopamine transporter, <sup>125</sup>
I PE2I and dopamine D2 receptors, <sup>125</sup>
I epidepride) and cholinergic (nicotinic α4β2 receptors, <sup>125</sup>
I 5IA85380 and muscarinic Ml receptors, <sup>3</sup>
H pirenzepine) parameters in the striatum and pallidum of pathologically confirmed PSP cases (n = 15) and controls (n = 32). In PSP, there was a marked loss of dopamine transporter and nicotinic α4β2 binding in the striatum and pallidum, consistent with loss of nigrostriatal neurones. Striatal D2 receptors were increased in the caudate and muscarinic Ml receptors were unchanged compared with controls. These results do not account for the poor response to dopaminergic and cholinergic replacement therapies in PSP, and suggest relative preservation of postsynaptic striatal projection neurones bearing D2/M1 receptors.</s0>
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	Movement Disorders (revue)
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Movement Disorders (revue)

Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy

Basal ganglia cholinergic and dopaminergic function in progressive supranuclear palsy

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