Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT
  Remyelination in multiple sclerosis : a new role for neurotrophins ?

Althaus, H. H. (2004). Remyelination in multiple sclerosis: a new role for neurotrophins? Progress in Brain Research, 146, 415-432. doi:10.1016/S0079-6123(03)46026-3.

Item is

Externe Referenzen

einblenden:

Urheber

einblenden:
ausblenden:
 Urheber:
Althaus, Hans Hinrich1, Autor           
Affiliations:
1Neural regeneration, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173663              

Inhalt

einblenden:
ausblenden:
Schlagwörter: neurotrophins; NGF; BNDF; remyelination; oligodendroglial cells; multiple sclerosis
 Zusammenfassung: Multiple sclerosis (MS) is a common neurological disease,which affects young adults. Its course is unpredictable and runs over decades. It is considered as an autoimmune disease, and is neuropathologically characterized by demyelination, variable loss of oligodendroglial cells, and axonal degeneration. Demyelination provides a permitting condition for axonal degeneration, which seems to be causative of permanent neurological deficits. Hence, the current treatment, which works preferentially immunmodulatory, should be complemented by therapeutics, which improves remyelination not only for restoring conduction velocity but also for preventing an irreversible axonal damage. One strategy to achieve this aim would be to promote remyelination by stimulating oligodendroglial cells remaining in MS lesions. While central nervous system neurons were already known to respond to neurotrophins (NT), interactions with glial cells became apparent more recently. In vitro and in vivo studies have shown that NT influence proliferation, differentiation, survival, and regeneration of mature oligodendrocytes and oligodendroglial precursors in favor of a myelin repair. Two in vivo models provided direct evidence that NT can improve remyelination. In addition, their neuroprotective and anti-inflammatory role would support a repair. Hence, a wealth of data point to NT as promising therapeutical candidates.

Details

einblenden:
ausblenden:
Sprache(n): eng - English
 Datum: 2004
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: eDoc: 213731
DOI: 10.1016/S0079-6123(03)46026-3
 Art des Abschluß: -

Veranstaltung

einblenden:

Entscheidung

einblenden:

Projektinformation

einblenden:

Quelle 1

einblenden:
ausblenden:
Titel: Progress in Brain Research
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: Amsterdam : Elsevier
Seiten: - Band / Heft: 146 Artikelnummer: - Start- / Endseite: 415 - 432 Identifikator: ISSN: 0079-6123
CoNE: https://pure.mpg.de/cone/journals/resource/954926958899