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Open AccessJournal ArticleDOI

Lithium inhibits Alzheimer's disease-like tau protein phosphorylation in neurons

TLDR
It is reported that lithium causes tau dephosphorylation at the sites recognized by antibodies Tau‐1 and PHF‐1 both in cultured neurons and in vivo in rat brain, consistent with a major role for glycogen synthase kinase‐3 in modifying proline‐directed sites on tau protein within living neurons under physiological conditions.
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This article is published in FEBS Letters.The article was published on 1997-07-14 and is currently open access. It has received 324 citations till now. The article focuses on the topics: Tau protein & GSK-3.

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Citations
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Journal ArticleDOI

The renaissance of GSK3.

TL;DR: Glycogen synthase kinase 3 was initially described as a key enzyme involved in glycogen metabolism, but is now known to regulate a diverse array of cell functions.
Journal ArticleDOI

The multifaceted roles of glycogen synthase kinase 3beta in cellular signaling.

TL;DR: GSK3beta has a central role regulating neuronal plasticity, gene expression, and cell survival, and may be a key component of certain psychiatric and neurodegenerative diseases.
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GSK3 takes centre stage more than 20 years after its discovery.

TL;DR: These latest findings have generated an enormous amount of interest in the development of drugs that inhibit GSK3 and which may have therapeutic potential for the treatment of diabetes, stroke and Alzheimer's disease.
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Decreased nuclear β‐catenin, tau hyperphosphorylation and neurodegeneration in GSK‐3β conditional transgenic mice

TL;DR: It is suggested that conditional transgenic mice overexpressing GSK‐3β in the brain during adulthood while avoiding perinatal lethality due to embryonic transgene expression can be used as an animal model to study the relevance of GSK-3β deregulation to the pathogenesis of Alzheimer's disease.
References
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Journal ArticleDOI

Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology

TL;DR: It is suggested that tau in Alzheimer brain is an abnormally phosphorylated protein component of PHF, the two major locations of paired-helical filaments in Alzheimer disease brain.
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A synthetic inhibitor of the mitogen-activated protein kinase cascade.

TL;DR: Results indicate that the MAPK pathway is essential for growth and maintenance of the ras-transformed phenotype and PD 098059 is an invaluable tool that will help elucidate the role of theMAPK cascade in a variety of biological settings.
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A molecular mechanism for the effect of lithium on development

TL;DR: It is shown that complete inhibition of IMPase has no effect on the morphogenesis of Xenopus embryos and a different hypothesis to explain the broad action of lithium is presented, which suggests that lithium acts through inhibition of glycogen synthase kinase-3 beta (GSK-3beta), which regulates cell fate determination in diverse organisms including Dictyostelium, Drosophila, and Xenopus.
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Microtubule-associated protein tau. A component of Alzheimer paired helical filaments.

TL;DR: Human brain tau and paired helical filament polypeptides co-migrated on sodium dodecyl sulfate-polyacrylamide gels suggest that tau is a major component of Alzheimer paired helicals filaments.
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Lithium inhibits glycogen synthase kinase-3 activity and mimics Wingless signalling in intact cells

TL;DR: Li+ acts as a specific inhibitor of the GSK-3 family of protein kinases in vitro and in intact cells, and mimics Wingless signalling, revealing a possible molecular mechanism of Li+ action on development and differentiation.
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