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Lithium neuroprotection: molecular mechanisms and clinical implications.
Expert Rev Mol Med. 2004 Oct 18; 6(21):1-18.ER

Abstract

Lithium has emerged as a neuroprotective agent efficacious in preventing apoptosis-dependent cellular death. Lithium neuroprotection is provided through multiple, intersecting mechanisms, although how lithium interacts with these mechanisms is still under investigation. Lithium increases cell survival by inducing brain-derived neurotrophic factor and thereby stimulating activity in anti-apoptotic pathways, including the phosphatidylinositol 3-kinase/Akt and the mitogen-activated protein kinase pathways. In addition, lithium reduces pro-apoptotic function by directly and indirectly inhibiting glycogen synthase kinase-3beta activity and indirectly inhibiting N-methyl-D-aspartate (NMDA)-receptor-mediated calcium influx. Lithium-induced regulation of anti- and pro-apoptotic pathways alters a wide variety of downstream effectors, including beta-catenin, heat shock factor 1, activator protein 1, cAMP-response-element-binding protein, and the Bcl-2 protein family. Lithium neuroprotection has a wide variety of clinical implications. Beyond its present use in bipolar mood disorder, lithium's neuroprotective abilities imply that it could be used to treat or prevent brain damage following traumatic injury, such as stroke, and neurodegenerative diseases such as Huntington's and Alzheimer's diseases.

Authors+Show Affiliations

Rowe MK
Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health Building 10, Room 4C206, 10 Center Drive, MSC 1363, Bethesda, MD 20892-1363, USA. mrowe@mail.nih.gov
Chuang DM
No affiliation info available

MeSH

Antimanic AgentsApoptosisBipolar DisorderBrain Damage, ChronicBrain InjuriesExcitatory Amino Acid AntagonistsFemaleGene Expression RegulationHumansLithiumMaleNerve Tissue ProteinsNeurodegenerative DiseasesNeuroprotective AgentsReceptors, N-Methyl-D-AspartateSignal TransductionStroke

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

15488156

Citation

Rowe, Michael K., and De-Maw Chuang. "Lithium Neuroprotection: Molecular Mechanisms and Clinical Implications." Expert Reviews in Molecular Medicine, vol. 6, no. 21, 2004, pp. 1-18.
Rowe MK, Chuang DM. Lithium neuroprotection: molecular mechanisms and clinical implications. Expert Rev Mol Med. 2004;6(21):1-18.
Rowe, M. K., & Chuang, D. M. (2004). Lithium neuroprotection: molecular mechanisms and clinical implications. Expert Reviews in Molecular Medicine, 6(21), 1-18.
Rowe MK, Chuang DM. Lithium Neuroprotection: Molecular Mechanisms and Clinical Implications. Expert Rev Mol Med. 2004 Oct 18;6(21):1-18. PubMed PMID: 15488156.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lithium neuroprotection: molecular mechanisms and clinical implications. AU - Rowe,Michael K, AU - Chuang,De-Maw, Y1 - 2004/10/18/ PY - 2004/10/19/pubmed PY - 2007/10/16/medline PY - 2004/10/19/entrez SP - 1 EP - 18 JF - Expert reviews in molecular medicine JO - Expert Rev Mol Med VL - 6 IS - 21 N2 - Lithium has emerged as a neuroprotective agent efficacious in preventing apoptosis-dependent cellular death. Lithium neuroprotection is provided through multiple, intersecting mechanisms, although how lithium interacts with these mechanisms is still under investigation. Lithium increases cell survival by inducing brain-derived neurotrophic factor and thereby stimulating activity in anti-apoptotic pathways, including the phosphatidylinositol 3-kinase/Akt and the mitogen-activated protein kinase pathways. In addition, lithium reduces pro-apoptotic function by directly and indirectly inhibiting glycogen synthase kinase-3beta activity and indirectly inhibiting N-methyl-D-aspartate (NMDA)-receptor-mediated calcium influx. Lithium-induced regulation of anti- and pro-apoptotic pathways alters a wide variety of downstream effectors, including beta-catenin, heat shock factor 1, activator protein 1, cAMP-response-element-binding protein, and the Bcl-2 protein family. Lithium neuroprotection has a wide variety of clinical implications. Beyond its present use in bipolar mood disorder, lithium's neuroprotective abilities imply that it could be used to treat or prevent brain damage following traumatic injury, such as stroke, and neurodegenerative diseases such as Huntington's and Alzheimer's diseases. SN - 1462-3994 UR - https://www.unboundmedicine.com/medline/citation/15488156/Lithium_neuroprotection:_molecular_mechanisms_and_clinical_implications_ DB - PRIME DP - Unbound Medicine ER -