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Lovastatin improves impaired LTP-like plasticity in patients with Neurofibromatosis Type 1

F. Mainberger, N. Jung, M. Zenker, I. Delvendahl, U. Wahlländer, L. Freudenberg, S. Berweck, T. Winkler, A. Straube, F. Heinen, V. Mall · Klinische Neurophysiologie · 2011 · Heft 03

Dokument
1078668
CareLit-ID
Jahr
2011
Publikation
PDF
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Metadaten
DOI
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Bibliografische Angaben

Zeitschrift
Klinische Neurophysiologie
Autor:innen
F. Mainberger, N. Jung, M. Zenker, I. Delvendahl, U. Wahlländer, L. Freudenberg, S. Berweck, T. Winkler, A. Straube, F. Heinen, V. Mall
Ausgabe
Heft 03 / 2011
Seiten
–
Erschienen: 2011-03-10 00:00:00
ISSN
1434-0275

Zusammenfassung

Neurofibromatosis Type 1 (NF1) is one of the most common genetic disorders that causes learning disabilities. In NF1 loss of function mutations of neurofibromin causes RAS-pathway hyperactivity, leading to deficits in long-term potentiation (LTP), a basic mechanism of learning and memory in the mouse model. Recently, it was shown that inhibition of HMG-CoA reductase by Lovastatin reduces RAS-pathway hyperactivity and improves LTP in NF1 mice. The presented study shows that humans with NF1 have impaired LTP-like plasticity and that this impairment can be rescued by Lovastatin. In 11 NF1-patients (28.0±9.2 y) and…

Schlagworte

Klinische Neurophysiologie