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Glycogen synthase kinase-3 in neurodegeneration and neuroprotection: lessons from lithium.
Curr Alzheimer Res. 2007 Feb; 4(1):21-31.CA

Abstract

For over fifty years lithium has been a fundamental component of therapy for patients with bipolar disorders. Lithium has been considered recently for its potential to alleviate neuronal loss and other neurodegeneration processes. For instance, lithium reduces the severity of some behavioral complications of Alzheimer's disease (AD). And there are growing indications that lithium may be of benefit to the underlying pathology of AD, as well as an array of other common CNS disorders, including stroke, Parkinson's disease, and Huntington's disease. Despite these demonstrated and prospective therapeutic benefits, lithium's mechanism of action remains elusive, and opinions differ regarding the most relevant molecular targets. Lithium inhibits several enzymes; significant among these are inositol monophosphatase (IMPase), glycogen synthase kinase-3 (GSK-3), and the proteasome. Most recent publications discussing the medical application of lithium have converged on GSK-3, so this article reviews data and discussions regarding the roles and interactions of GSK-3 with other proteins and its proposed role in the pathogenesis of Alzheimer's disease.

Authors+Show Affiliations

School of Biology, University of Tehran, Tehran 14155-6455, Iran.No affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

17316163

Citation

Aghdam, Saeed Yadranji, and Steven W. Barger. "Glycogen Synthase Kinase-3 in Neurodegeneration and Neuroprotection: Lessons From Lithium." Current Alzheimer Research, vol. 4, no. 1, 2007, pp. 21-31.
Aghdam SY, Barger SW. Glycogen synthase kinase-3 in neurodegeneration and neuroprotection: lessons from lithium. Curr Alzheimer Res. 2007;4(1):21-31.
Aghdam, S. Y., & Barger, S. W. (2007). Glycogen synthase kinase-3 in neurodegeneration and neuroprotection: lessons from lithium. Current Alzheimer Research, 4(1), 21-31.
Aghdam SY, Barger SW. Glycogen Synthase Kinase-3 in Neurodegeneration and Neuroprotection: Lessons From Lithium. Curr Alzheimer Res. 2007;4(1):21-31. PubMed PMID: 17316163.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glycogen synthase kinase-3 in neurodegeneration and neuroprotection: lessons from lithium. AU - Aghdam,Saeed Yadranji, AU - Barger,Steven W, PY - 2007/2/24/pubmed PY - 2007/3/28/medline PY - 2007/2/24/entrez SP - 21 EP - 31 JF - Current Alzheimer research JO - Curr Alzheimer Res VL - 4 IS - 1 N2 - For over fifty years lithium has been a fundamental component of therapy for patients with bipolar disorders. Lithium has been considered recently for its potential to alleviate neuronal loss and other neurodegeneration processes. For instance, lithium reduces the severity of some behavioral complications of Alzheimer's disease (AD). And there are growing indications that lithium may be of benefit to the underlying pathology of AD, as well as an array of other common CNS disorders, including stroke, Parkinson's disease, and Huntington's disease. Despite these demonstrated and prospective therapeutic benefits, lithium's mechanism of action remains elusive, and opinions differ regarding the most relevant molecular targets. Lithium inhibits several enzymes; significant among these are inositol monophosphatase (IMPase), glycogen synthase kinase-3 (GSK-3), and the proteasome. Most recent publications discussing the medical application of lithium have converged on GSK-3, so this article reviews data and discussions regarding the roles and interactions of GSK-3 with other proteins and its proposed role in the pathogenesis of Alzheimer's disease. SN - 1567-2050 UR - https://www.unboundmedicine.com/medline/citation/17316163/Glycogen_synthase_kinase_3_in_neurodegeneration_and_neuroprotection:_lessons_from_lithium_ L2 - https://www.eurekaselect.com/77773/article DB - PRIME DP - Unbound Medicine ER -