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Microtubule-associated Protein Tau, Paired Helical Filaments, and Phosphorylation (1993)

MANDELKOW, E.-M. ; BIERNAT, J. ; DREWES, G. ; [et al.]

Oxford, UK : Blackwell Publishing Ltd

Annals of the New York Academy of Sciences 695 (1993), S. 0

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ISSN: 1749-6632

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Natural Sciences in General

Notes: This paper summarizes our recent studies on microtubule-associated protein tau and its pathological state resembling that of the paired helical filaments of Alzheimer's disease. The Alzheimer-like state of tau protein can be identified and analyzed in terms of certain phosphorylation sites and phosphorylation-dependent antibody epitopes. It can be induced by protein kinases which tend to phosphorylate serine or threonine residues followed by a proline; this includes mitogen-activated protein kinase (MAPK) and glycogen-synthase kinase 3 (GSK-3). Both of these are tightly associated with microtubules as well as with paired helical filaments. Structurally, tau appears as a rod-like molecule; it tends to self-associate into dimers whose monomers are antiparallel. Constructs of truncated tau made up of antiparallel dimers of the microtubule binding domain can be assembled into paired helical filaments in vitro.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23054.x

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Evidence for prolonged recovery of dopaminergic transmission after detoxification in alcoholics with poor treatment outcome (1995)

Heinz, A. ; Lichtenberg-Kraag, B. ; Sällström Baum, S. ; [et al.]

Springer

Journal of neural transmission 102 (1995), S. 149-157

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ISSN: 1435-1463

Keywords: Dopamine receptors ; Growth Hormone ; alcoholism ; dopamine ; relapse ; neuroadaption

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Summary It has been hypothesized that dysfunction of dopaminergic neurotransmission is involved in the pathogenesis of alcohol addiction. Therefore, peripheral dopamine levels, sensitivity of central dopamine receptors (apomorphine-induced Growth Hormone (GH) secretion), and the inhibitory efficacy of G-proteins on adenylyl cyclase activity (as an indicator for dopamine D2-receptor coupled second messenger mechanisms) were measured in 45 alcohol-dependent patients before and after detoxification and in 10 healthy controls. The time needed to adjust to abstinence conditions differed between patients with good and poor treatment outcome. In subsequent abstainers, effects of alcohol withdrawal were already found during the first 24 hours of abstinence (normalisation of GH response, increases in dopamine levels and the inhibitory efficacy of G-proteins). During the next 7 days of abstinence, no more significant changes were observed in the assessed variables. In subsequent relapsers, no significant effect of acute ethanol withdrawal on the same measures was found. However, at day 8 of abstinence, increases in apomorphine-induced GH secretion (towards normalisation), in dopamine plasma levels, and in the inhibitory efficacy of G-proteins (towards above-normal levels) were observed. This retarded adjustment of dopaminergic signal transduction seems to reflect the relapse risk of treatment non-responders.