Kainate-induced toxicity in the hippocampus: potential role of lithium.
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Summary
A robust neuroprotective effect of lithium in the excitotoxic process induced by KA in mouse hippocampus was demonstrated via modulation of calcium entry and the subsequent inhibition of the calpain pathway, suggesting that it may be useful as a possible therapeutic strategy for Alzheimer's disease.
- Type
- article
- Published
- 2010-06-01
- Cited by
- 14
- References
- 44
- OpenAlex
- https://openalex.org/W20636640
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:25455822
Keywords
Computer science
References
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- Lithium Treatment Decreases Activities of Tau Kinases in a Murine Model of Senescence
- Prevention of MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) dopaminergic neurotoxicity in mice by chronic lithium: involvements of Bcl-2 and Bax.
- Akt as a mediator of cell death
- Neuroprotective Effects of Regulators of the Glycogen Synthase Kinase-3β Signaling Pathway in a Transgenic Model of Alzheimer's Disease Are Associated with Reduced Amyloid Precursor Protein Phosphorylation
- Glutamate-induced neuronal death: a succession of necrosis or apoptosis depending on mitochondrial function.
- Increased sensitivity to N-methyl-D-aspartate receptor-mediated excitotoxicity in a mouse model of Huntington's disease.
- Inactivation of glycogen synthase kinase-3beta protects against kainic acid-induced neurotoxicity in vivo.
- Lithium reduces tau phosphorylation but not A beta or working memory deficits in a transgenic model with both plaques and tangles.
- Axonal remodeling and synaptic differentiation in the cerebellum is regulated by WNT-7a signaling.
- Inhibition of calpain and caspase-3 prevented apoptosis and preserved electrophysiological properties of voltage-gated and ligand-gated ion channels in rat primary cortical neurons exposed to glutamate.
- Enhanced Sensitivity of “Metabotropic” Glutamate Receptors After Induction of Long‐Term Potentiation in Rat Hippocampus
- Glutamate neurotoxicity and diseases of the nervous system.
Cited by
- Potential Mechanisms of Action of Lithium in Bipolar Disorder
- Excitotoxicity induced by kainic acid provokes glycogen synthase kinase-3 truncation in the hippocampus.
- Possible Role of the Glycogen Synthase Kinase-3 Signaling Pathway in Trimethyltin-Induced Hippocampal Neurodegeneration in Mice
- Antiepileptogenic effect of curcumin on kainate-induced model of temporal lobe epilepsy
- CDK5 activator protein p25 preferentially binds and activates GSK3β
- Cerebrospinal fluid protein biomarker panel for assessment of neurotoxicity induced by kainic acid in rats.
- Melatonin Mediates Protective Effects against Kainic Acid-Induced Neuronal Death through Safeguarding ER Stress and Mitochondrial Disturbance
- Melatonin Mitigates Kainic Acid-Induced Neuronal Tau Hyperphosphorylation and Memory Deficits through Alleviating ER Stress
- Potential mechanisms underlying lithium treatment for Alzheimer’s disease and COVID-19
- Lithium in Cancer Therapy: Friend or Foe?
- Running title: Potential Mechanisms of Action of Lithium in Bipolar Disorder Potential Mechanisms of Action of Lithium in Bipolar Disorder Current Understanding
- Recerca en Biomedicina
- Bivalent Cations in Bipolar Disorders
- CDK 5 activator protein p 25 preferentially binds and activates GSK 3 β
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