Zusammenfassung
Trotz vieler neuer Erkenntnisse ist die Pathogenese der DAT noch immer weitgehend ungeklärt. Wahrscheinlich ist, daß es sich bei der phänomenologisch relativ homogenen DAT pathophysiologisch um eine heterogene Erkrankung handelt, bei der verschiedene neurodegenerative Prozesse und kompensatorische „plastische“ Vorgänge interagieren. Neben genetischen Faktoren werden u. a. auch erworbene Störungen des Zellstoffwechsels als Grundlage der Erkrankung diskutiert (St George-Hyslop et al. 1990, Hardy 1992, Kosik 1992, Blass 1993). Verminderungen in der regionalen zerebralen Glukoseutilisation bei der DAT gehören zu den am besten dokumentierten Untersuchungen und wurden bereits 1978 von Hoyer erstmalig beschrieben (Hoyer 1978). Gleichzeitig konnte gezeigt werden, daß die bidirektionelle Kapazität des Glukosetransportes über die Blut-Hirn-Schranke nicht beeinträchtigt ist (Friedland et al. 1989), obwohl in biochemischen Untersuchungen eine Reduktion von Glukosetransportern sowohl in der Blut-Hirn-Schranke (Kalaria und Harik 1989) als auch im Gehirngewebe (Simpson et al. 1994) bei DAT bewiesen wurde. Mittels Positronen-Emissionstomographie (PET) ließen sich unter Verwendung von [18Fluor]-markierter Desoxyglukose regelmäßig Reduktionen der Utilisation nachweisen und zwar im parieto-temporalen Übergangskortex (de Leon et al. 1983, Ferris et al. 1983, Haxby et al. 1986, Friedland et al. 1989). Biochemische Untersuchungen lieferten ebenfalls Hinweise auf einen gestörten Glukosemetabolismus.
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Blum-Degen, D., Frölich, L., Hoyer, S., Riederer, P. (1996). Insulinrezeptoren im menschlichen post-mortalen Hirnkortex bei normaler Alterung und bei Demenz vom Alzheimer-Typ. In: Möller, HJ., Müller-Spahn, F., Kurtz, G. (eds) Aktuelle Perspektiven der Biologischen Psychiatrie. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6889-9_9
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