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  • 1
    ISSN: 1433-0407
    Keywords: Schlüsselwörter ALS ; Neurogenetik ; Exzitatorische Aminosäuren ; Cu/Zn-SOD ; Key words Amyotrophic lateral sclerosis ; Neurogenetics ; Excitatory amino acids ; Cu/Zn SOD
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary At presently, the etiology and pathogenesis of amyotrophic lateral sclerosis (ALS) are unknown. In recent years, the genetic background of hereditary motor neuron diseases has been partly defined. In particular, these advances represent an opportunity to improve our understanding of the pathogenesis of the familial and sporadic forms of ALS and thus provide a basis for rational therapeutic approaches. In this article, recent findings on the pathogenesis of the familial form of ALS and their implications for the sporadic form are discussed.
    Notes: Zusammenfassung Die Ätiologie und Pathogenese der amyotrophen Lateralsklerose (ALS) bleibt weitgehend ungeklärt. In den zurückliegenden Jahren sind bei den genetisch bedingten Varianten dieser Erkrankung wichtige Fortschritte bei der Identifizierung ihrer molekularbiologischen Grundlagen gemacht worden. Diese Fortschritte berechtigen zu der Hoffnung, daß es in Zukunft gelingt, die Pathogenese der familiären, aber auch der sporadischen Formen der Erkrankung zu erhellen und damit rationalen Therapieansätzen weiter den Weg zu bereiten. Im Rahmen dieser Übersichtsarbeit soll sowohl auf die vorliegenden Befunde bei der familiären Form der ALS (fALS) als auch auf die mögliche Bedeutung dieser Befunde für pathogenetische Vorstellungen bei der sporadischen Form der ALS (sALS) eingegangen werden.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1619-7089
    Keywords: Partial epilepsy ; SPET ; Benzodiazepine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It was the aim of this study to compare benzodiazepine (Bz) receptor binding and cerebral perfusion in patients with partial epilepsy. Single photon emission tomography (SPET) studies with the flow-marker technetium 99m hexamethylpropylene amine oxine (99mTc-HMPAO) and with the 123I-labelled Bz-receptor ligand Ro 16-0154 (123I-Iomazenil) were performed in 12 patients with partial epilepsy, all with normal magnetic resonance imaging (MRI) and computed tomography (CT) scans. The SPET studies with 123I-Iomazenil were carried out 5 min and 2 h after injection. At 2 h the distribution of activity was very similar to the expected distribution of Bz-receptors in the human brain, known from positron emission tomography (PET) work and post-mortem studies. Early images showed a significantly higher tracer accumulation in the area of the basal ganglia, cerebellum, and naso-pharyngeal space. This finding is caused by non-specific binding and the contribution of the tracer in the blood pool in this phase. Also after 2 h p.i. of 123I-Iomazenil, 9 of the 12 patients showed a focal decrease of of Bz-receptor binding. Ten patients had focal flow abnormalities with 99mTc-HMPAO SPET. In 8 subjects impairment of flow was seen in sites of reduced 123I-Iomazenil uptake. 123I-Io-mazenil is suitable for Bz-receptor mapping. In this series of patients, Bz-receptor mapping with SPET seems to offer no advantage over 99mTc-HMPAO in the detection of epileptic foci.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1619-7089
    Keywords: Partial epilepsy ; SPET ; Benzodiazepine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It was the aim of this study to compare benzodiazepine (Bz) receptor binding and cerebral perfusion in patients with partial epilepsy. Single photon emission tomography (SPET) studies with the flow-marker technetium 99m hexamethylpropylene amine oxine (99mTc-HMPAO) and with the123I-labelled Bz-receptor ligand Ro 16-0154 (123I-Iomazenil) were performed in 12 patients with partial epilepsy, all with normal magnetic resonance imaging (MRI) and computed tomography (CT) scans. The SPET studies with123I-Iomazenil were carried out 5 min and 2 h after injection. At 2 h the distribution of activity was very similar to the expected distribution of Bz-receptors in the human brain, known from positron emission tomography (PET) work and post-mortem studies. Early images showed a significantly higher tracer accumulation in the area of the basal ganglia, cerebellum, and naso-pharyngeal space. This finding is caused by non-specific binding and the contribution of the tracer in the blood pool in this phase. Also after 2 h p.i. of123I-Iomazenil, 9 of the 12 patients showed a focal decrease of of Bz-receptor binding. Ten patients had focal flow abnormalities with99mTc-HMPAO SPET. In 8 subjects impairment of flow was seen in sites of reduced123I-Iomazenil uptake.123I-Io-mazenil is suitable for Bz-receptor mapping. In this series of patients, Bz-receptor mapping with SPET seems to offer no advantage over99mTc-HMPAO in the detection of epileptic foci.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1459
    Keywords: Key words Amyotrophic lateral sclerosis ; Cu/Zn SOD ; EAAT2 ; AMPA ; Neurolathyrism ; Riluzole
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is well accepted that excitotoxic mechanisms contribute to the pathogenesis of acute neuronal death in stroke, epilepsy, or brain trauma. It is less widely acknowledged that excitotoxic mechanisms play a role in the pathogenesis of chronic neurological disorders, in particular neurodegenerative diseases. However, evidence is accumulating that this mechanism is indeed part of the pathogenesis of late-onset neurodegenerative diseases. One of the clinical examples may be amyotrophic lateral sclerosis, a disease in which antiexcitotoxic strategies have neuroprotective effects in both, an established animal model and in man. In addition, there is accumulating neuropathological, pathobiochemical and pathophysiological evidence which indicates that excitotoxic mechanisms are part of the pathogenesis of the human disease and consequently part of the mechanisms explaining selective vulnerability (“pathoclisis”) in the human motor system.
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