MovDisordV3, PascalFrancis, Corpus, bibRecord, 001A16

Iron metabolism in Parkinsonian syndromes

Identifieur interne : 001A16 ( PascalFrancis/Corpus ); précédent : 001A15; suivant : 001A17

Iron metabolism in Parkinsonian syndromes

Auteurs : Daniela Berg ; Helmine Hochstrasser

Source :

Movement disorders [ 0885-3185 ] ; 2006.

RBID : Pascal:06-0518080

Descripteurs français

Pascal (Inist)
- Système nerveux pathologie, Parkinson maladie, Fer, Métabolisme, Noyau gris central, Trouble fonctionnel.

English descriptors

KwdEn :
- Basal ganglion, Dysfunction, Iron, Metabolism, Nervous system diseases, Parkinson disease.

Abstract

Growing evidence suggests an involvement of iron in the pathophysiology of neurodegenerative diseases. Several of the diseases are associated with parkinsonian syndromes, induced by degeneration of basal ganglia regions that contain the highest amount of iron within the brain. The group of neurodegenerative disorders associated with parkinsonian syndromes with increased brain iron content can be devided into two groups: (1) parkinsonian syndromes associated with brain iron accumulation, including Parkinson disease, diffuse Lewy body disease, parkinsonian type of multiple system atrophy, progressive supranuclear palsy, corticobasal ganglionic degeneration, and Westphal variant of Huntington's disease; and (2) monogenetically caused disturbances of brain iron metabolism associated with parkinsonian syndromes, including aceruloplasminemia, hereditary ferritinopathies affecting the basal ganglia, and panthotenate kinase associated neurodegeneration type 2. Although it is still a matter of debate whether iron accumulation is a primary cause or secondary event in the first group, there is no doubt that iron-induced oxidative stress contributes to neurodegeneration. Parallels concerning pathophysiological as well as clinical aspects can be drawn between disorders of both groups. Results from animal models and reduction of iron overload combined with at least partial relief of symptoms by application of iron chelators in patients of the second group give hope that targeting the iron overload might be one possibility to slow down the neurodegenerative cascade also in the first group of inevitably progressive neurodegenerative disorders.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 Growing evidence suggests an involvement of iron in the pathophysiology of neurodegenerative diseases. Several of the diseases are associated with parkinsonian syndromes, induced by degeneration of basal ganglia regions that contain the highest amount of iron within the brain. The group of neurodegenerative disorders associated with parkinsonian syndromes with increased brain iron content can be devided into two groups: (1) parkinsonian syndromes associated with brain iron accumulation, including Parkinson disease, diffuse Lewy body disease, parkinsonian type of multiple system atrophy, progressive supranuclear palsy, corticobasal ganglionic degeneration, and Westphal variant of Huntington's disease; and (2) monogenetically caused disturbances of brain iron metabolism associated with parkinsonian syndromes, including aceruloplasminemia, hereditary ferritinopathies affecting the basal ganglia, and panthotenate kinase associated neurodegeneration type 2. Although it is still a matter of debate whether iron accumulation is a primary cause or secondary event in the first group, there is no doubt that iron-induced oxidative stress contributes to neurodegeneration. Parallels concerning pathophysiological as well as clinical aspects can be drawn between disorders of both groups. Results from animal models and reduction of iron overload combined with at least partial relief of symptoms by application of iron chelators in patients of the second group give hope that targeting the iron overload might be one possibility to slow down the neurodegenerative cascade also in the first group of inevitably progressive neurodegenerative disorders.
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Format Inist (serveur)

NO :	PASCAL 06-0518080 INIST
ET :	Iron metabolism in Parkinsonian syndromes
AU :	BERG (Daniela); HOCHSTRASSER (Helmine)
AF :	Hertie Institute of Clinical Brain Research and Department of Medical Genetics, University of Tubingen/Allemagne (1 aut.); Department of Medical Genetics, University of Tubingen/Allemagne (2 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2006; Vol. 21; No. 9; Pp. 1299-1310; Bibl. 181 ref.
LA :	Anglais
EA :	Growing evidence suggests an involvement of iron in the pathophysiology of neurodegenerative diseases. Several of the diseases are associated with parkinsonian syndromes, induced by degeneration of basal ganglia regions that contain the highest amount of iron within the brain. The group of neurodegenerative disorders associated with parkinsonian syndromes with increased brain iron content can be devided into two groups: (1) parkinsonian syndromes associated with brain iron accumulation, including Parkinson disease, diffuse Lewy body disease, parkinsonian type of multiple system atrophy, progressive supranuclear palsy, corticobasal ganglionic degeneration, and Westphal variant of Huntington's disease; and (2) monogenetically caused disturbances of brain iron metabolism associated with parkinsonian syndromes, including aceruloplasminemia, hereditary ferritinopathies affecting the basal ganglia, and panthotenate kinase associated neurodegeneration type 2. Although it is still a matter of debate whether iron accumulation is a primary cause or secondary event in the first group, there is no doubt that iron-induced oxidative stress contributes to neurodegeneration. Parallels concerning pathophysiological as well as clinical aspects can be drawn between disorders of both groups. Results from animal models and reduction of iron overload combined with at least partial relief of symptoms by application of iron chelators in patients of the second group give hope that targeting the iron overload might be one possibility to slow down the neurodegenerative cascade also in the first group of inevitably progressive neurodegenerative disorders.
CC :	002B17; 002B17D; 002B23E
FD :	Système nerveux pathologie; Parkinson maladie; Fer; Métabolisme; Noyau gris central; Trouble fonctionnel
FG :	Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux central
ED :	Nervous system diseases; Parkinson disease; Iron; Metabolism; Basal ganglion; Dysfunction
EG :	Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Central nervous system
SD :	Sistema nervioso patología; Parkinson enfermedad; Hierro; Metabolismo; Núcleo basal; Trastorno funcional
LO :	INIST-20953.354000158780860010
ID :	06-0518080

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Pascal:06-0518080

Le document en format XML

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<AU>BERG (Daniela); HOCHSTRASSER (Helmine)</AU>
<AF>Hertie Institute of Clinical Brain Research and Department of Medical Genetics, University of Tubingen/Allemagne (1 aut.); Department of Medical Genetics, University of Tubingen/Allemagne (2 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
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   |texte=   Iron metabolism in Parkinsonian syndromes
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	Movement Disorders (revue)
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Movement Disorders (revue)

Iron metabolism in Parkinsonian syndromes

Iron metabolism in Parkinsonian syndromes

Source :

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Abstract

Notice en format standard (ISO 2709)

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