Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Der Nervenarzt 68 (1997), S. 785-791 
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 247 (2000), S. I7 
    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.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of inherited metabolic disease 16 (1993), S. 716-723 
    ISSN: 1573-2665
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary There is increasing evidence that the neurotoxic effects of excitatory amino acids and their analogues are part of the pathogenesis of neuronal degeneration in acute and chronic neurological disease. Recent studies indicate that activation of excitatory amino acid receptors is also induced in the mechanism of neuronal damage induced by impairment of cellular energy metabolism. This article briefly summarizes the evidence for the presence of such a mechanism and discusses metabolic diseases in which excitatory amino acids alone or in combination with energy deficiency could play a pathogenetic role. In these and other metabolic diseases, antagonists to excitatory amino acid receptors may offer a therapeutic opportunity; however, there are potential limits that may prevent chronic use.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...