MovDisordV3, Main, Exploration, bibRecord, 000C94

New Synaptic and Molecular Targets for Neuroprotection in Parkinson’s Disease

Identifieur interne : 000C94 ( Main/Exploration ); précédent : 000C93; suivant : 000C95

New Synaptic and Molecular Targets for Neuroprotection in Parkinson’s Disease

Auteurs : Paolo Calabresi [Italie] ; Massimiliano Di Filippo [Italie] ; Antongiulio Gallina [Italie] ; Yingfei Wang [États-Unis] ; Jeannette N. Stankowski [États-Unis] ; Barbara Picconi [Italie] ; Valina L. Dawson [États-Unis] ; Ted M. Dawson [États-Unis]

Source :

Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2012.

RBID : PMC:4161019

English descriptors

KwdEn :
- Humans, Neurons (drug effects), Neurons (pathology), Neuroprotective Agents (therapeutic use), Parkinson Disease (drug therapy), Parkinson Disease (genetics), Parkinson Disease (pathology), Protein-Serine-Threonine Kinases (genetics), Protein-Serine-Threonine Kinases (metabolism), Receptor, Adenosine A2A (metabolism), Receptors, Dopamine (metabolism), Receptors, N-Methyl-D-Aspartate (metabolism), Signal Transduction (drug effects), Synapses (drug effects), Synapses (pathology).
MESH :
- chemical , genetics : Protein-Serine-Threonine Kinases.
- chemical , metabolism : Protein-Serine-Threonine Kinases, Receptor, Adenosine A2A, Receptors, Dopamine, Receptors, N-Methyl-D-Aspartate.
- chemical , therapeutic use : Neuroprotective Agents.
- drug effects : Neurons, Signal Transduction, Synapses.
- drug therapy : Parkinson Disease.
- genetics : Parkinson Disease.
- pathology : Neurons, Parkinson Disease, Synapses.
- Humans.

Abstract

The defining anatomical feature of Parkinson’s disease (PD) is the degeneration of substantia nigra pars compacta (SNc) neurons, resulting in striatal dopamine (DA) deficiency and in the subsequent alteration of basal ganglia physiology. Treatments targeting the dopaminergic system alleviate PD symptoms but are not able to slow the neurodegenerative process that underlies PD progression. The nucleus striatum comprises a complex network of projecting neurons and interneurons that integrates different neural signals to modulate the activity of the basal ganglia circuitry. In this review we describe new potential molecular and synaptic striatal targets for the development of both symptomatic and neuroprotective strategies for PD. In particular, we focus on the interaction between adenosine A2A receptors and dopamine D2 receptors, on the role of a correct assembly of NMDA receptors, and on the sGC/cGMP/PKG pathway. Moreover, we also discuss the possibility to target the cell death program parthanatos and the kinase LRRK2 in order to develop new putative neuroprotective agents for PD acting on dopaminergic nigral neurons as well as on other basal ganglia structures.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161019

DOI: 10.1002/mds.25096
PubMed: 22927178
PubMed Central: 4161019

Affiliations:

Le document en format XML

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<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (pathology)</term>
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<front><div type="abstract" xml:lang="en"><p id="P1">The defining anatomical feature of Parkinson’s disease (PD) is the degeneration of substantia nigra pars compacta (SNc) neurons, resulting in striatal dopamine (DA) deficiency and in the subsequent alteration of basal ganglia physiology. Treatments targeting the dopaminergic system alleviate PD symptoms but are not able to slow the neurodegenerative process that underlies PD progression. The nucleus striatum comprises a complex network of projecting neurons and interneurons that integrates different neural signals to modulate the activity of the basal ganglia circuitry. In this review we describe new potential molecular and synaptic striatal targets for the development of both symptomatic and neuroprotective strategies for PD. In particular, we focus on the interaction between adenosine A2A receptors and dopamine D2 receptors, on the role of a correct assembly of NMDA receptors, and on the sGC/cGMP/PKG pathway. Moreover, we also discuss the possibility to target the cell death program parthanatos and the kinase LRRK2 in order to develop new putative neuroprotective agents for PD acting on dopaminergic nigral neurons as well as on other basal ganglia structures.</p>
</div>
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Movement Disorders (revue)

New Synaptic and Molecular Targets for Neuroprotection in Parkinson’s Disease

New Synaptic and Molecular Targets for Neuroprotection in Parkinson’s Disease

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki

	Movement Disorders (revue)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.