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Glycogen synthase kinase-3beta, or a link between amyloid and tau pathology?
Genes Brain Behav. 2008 Feb; 7 Suppl 1:57-66.GB

Abstract

Phosphorylation is the most common post-translational modification of cellular proteins, essential for most physiological functions. Deregulation of phosphorylation has been invoked in disease mechanisms, and the case of Alzheimer's disease (AD) is no exception: both in the amyloid pathology and in the tauopathy are kinases deeply implicated. The glycogen synthase kinase-3 (GSK-3) isozymes participate in diverse cellular processes and important signalling pathways and have been implicitly linked to diverse medical problems, i.e. from diabetes and cancer to mood disorders and schizophrenia, and in the neurodegeneration of AD. Here, we review specific aspects of GSK-3 isozymes in the framework of recent data that we obtained in novel transgenic mouse models that robustly recapitulate the pathology and mechanistical problems of AD.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Muyllaert D
Experimental Genetics Group, K.U. Leuven, Leuven, Belgium.
Kremer A
No affiliation info available
Jaworski T
No affiliation info available
Borghgraef P
No affiliation info available
Devijver H
No affiliation info available
Croes S
No affiliation info available
Dewachter I
No affiliation info available
Van Leuven F
No affiliation info available

MeSH

Alzheimer DiseaseAmyloidAnimalsDisease Models, AnimalGlycogen Synthase Kinase 3HumansIsoenzymesLithiumMiceMice, TransgenicPhosphorylationTauopathiestau Proteins

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

18184370

Citation

Muyllaert, D, et al. "Glycogen Synthase Kinase-3beta, or a Link Between Amyloid and Tau Pathology?" Genes, Brain, and Behavior, vol. 7 Suppl 1, 2008, pp. 57-66.
Muyllaert D, Kremer A, Jaworski T, et al. Glycogen synthase kinase-3beta, or a link between amyloid and tau pathology? Genes Brain Behav. 2008;7 Suppl 1:57-66.
Muyllaert, D., Kremer, A., Jaworski, T., Borghgraef, P., Devijver, H., Croes, S., Dewachter, I., & Van Leuven, F. (2008). Glycogen synthase kinase-3beta, or a link between amyloid and tau pathology? Genes, Brain, and Behavior, 7 Suppl 1, 57-66. https://doi.org/10.1111/j.1601-183X.2007.00376.x
Muyllaert D, et al. Glycogen Synthase Kinase-3beta, or a Link Between Amyloid and Tau Pathology. Genes Brain Behav. 2008;7 Suppl 1:57-66. PubMed PMID: 18184370.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glycogen synthase kinase-3beta, or a link between amyloid and tau pathology? AU - Muyllaert,D, AU - Kremer,A, AU - Jaworski,T, AU - Borghgraef,P, AU - Devijver,H, AU - Croes,S, AU - Dewachter,I, AU - Van Leuven,F, PY - 2008/2/8/pubmed PY - 2008/3/13/medline PY - 2008/2/8/entrez SP - 57 EP - 66 JF - Genes, brain, and behavior JO - Genes Brain Behav VL - 7 Suppl 1 N2 - Phosphorylation is the most common post-translational modification of cellular proteins, essential for most physiological functions. Deregulation of phosphorylation has been invoked in disease mechanisms, and the case of Alzheimer's disease (AD) is no exception: both in the amyloid pathology and in the tauopathy are kinases deeply implicated. The glycogen synthase kinase-3 (GSK-3) isozymes participate in diverse cellular processes and important signalling pathways and have been implicitly linked to diverse medical problems, i.e. from diabetes and cancer to mood disorders and schizophrenia, and in the neurodegeneration of AD. Here, we review specific aspects of GSK-3 isozymes in the framework of recent data that we obtained in novel transgenic mouse models that robustly recapitulate the pathology and mechanistical problems of AD. SN - 1601-183X UR - https://www.unboundmedicine.com/medline/citation/18184370/Glycogen_synthase_kinase_3beta_or_a_link_between_amyloid_and_tau_pathology DB - PRIME DP - Unbound Medicine ER -