Implication of cyclin-dependent kinase 5 in the neuroprotective properties of lithium

Jordà, Elvira G.; Verdaguer, Ester; Canudas, Anna Maria; Jiménez, Andrés; Arriba, Susana Garcia de; Allgaier, Clemens; Pallàs, Mercè; Camins, Antoni

doi:10.1016/j.neuroscience.2005.04.061

Cited by 35 publications

(24 citation statements)

References 43 publications

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“…Since the pioneering studies of D'Mello et al (5) and Volonte et al (6) in 1994, it has become increasingly evident that lithium displays neuroprotective effects against cell injuries caused by a variety of noxious insults in cultured cells (Table 1), as well as animal models of various neurodegenerative diseases and human patients with manic-depressive illness (Table 2). These insults include ischemia (7,8), glutamate excitotoxicity (9 -16), β-amyloid (17 -23), C 2 -ceramide (24), colchicine (25), growth factor withdrawal (26), switching of high K + to normal K + medium (5,27), irradiation (28), exposure to heat shock (29), high dose of anticonvulsants (30), Bungarus multicinctus β-bungarotoxin (31), animal model of Alzheimer's disease (21), in vitro (32) and in vivo (33) models of Parkinson's disease, animal models of Huntington's disease (34 -36), tauopathies caused by tau protein (37 -39), and thapsigargin-induced, cytoplasmic Ca 2+ overload-mediated, endoplasmic reticulum (ER) stress (40).…”

Section: Introductionmentioning

confidence: 99%

“…Although the functional relationship between Ser-phosphorylation and Tyrphosphorylation of GSK-3α/ 3β for regulating catalytic activity of GSK-3α/ 3β is not satisfactorily elucidated (56), their study may implicate that Ser 9 -phosphorylation of GSK-3β is sufficient to override GSK-3β activation by Tyr 216 -phosphorylation. Colchicine-induced apoptosis in cerebellar granule cells is a model of programmed cell death mediated by cytoskeletal derangement, associated with release of various pro-apoptotic molecules from mitochondria (25). In cultured rat cerebellar granule cells, Jordà et al (25) showed that colchicine treatment (1 µM for 24 h) caused Ser…”

mentioning

confidence: 99%

“…Colchicine-induced apoptosis in cerebellar granule cells is a model of programmed cell death mediated by cytoskeletal derangement, associated with release of various pro-apoptotic molecules from mitochondria (25). In cultured rat cerebellar granule cells, Jordà et al (25) showed that colchicine treatment (1 µM for 24 h) caused Ser…”

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confidence: 99%

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Lithium: Potential Therapeutics Against Acute Brain Injuries and Chronic Neurodegenerative Diseases

et al. 2005

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Abstract. In addition to the well-documented mood-stabilizing effects of lithium in manicdepressive illness patients, recent in vitro and in vivo studies in rodents and humans have increasingly implicated that lithium can be used in the treatment of acute brain injuries (e.g., ischemia) and chronic neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, tauopathies, and Huntington's disease). Consistent with this novel view, substantial evidences suggest that depressive illness is not a mere neurochemical disease, but is linked to gray matter atrophy due to the reduced number / size of neurons and glia in brain. Importantly, neurogenesis, that is, birth / maturation of functional new neurons, continues to occur throughout the lifetime in human adult brains (e.g., hippocampus); the neurogenesis is impaired by multiple not-fully defined factors (e.g., aging, chronic stress-induced increase of glucocorticoids, and excitotoxicity), accounting for brain atrophy in patients with depressive illness and neurodegenerative diseases. Chronic treatment of lithium, in agreement with the delayed-onset of mood-stabilizing effects of lithium, up-regulates cell survival molecules (e.g., Bcl-2, cyclic AMP-responsive element binding protein, brain-derived neurotrophic factor, Grp78, Hsp70, and β-catenin), while down-regulating pro-apoptotic activities (e.g., excitotoxicity, p53, Bax, caspase, cytochrome c release, β-amyloid peptide production, and tau hyperphosphorylation), thus preventing or even reversing neuronal cell death and neurogenesis retardation.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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Lithium: Potential Therapeutics Against Acute Brain Injuries and Chronic Neurodegenerative Diseases

et al. 2005

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“…Their neuroprotective properties have also been demonstrated in primary cultures of neurons [42,43,44]. The fact that they also afford protection against the neurotoxic effects of ALS/CSF on MCN cultures (fig.…”

Section: Discussionmentioning

confidence: 98%

The Neuroprotection Exerted by Memantine, Minocycline and Lithium, against Neurotoxicity of CSF from Patients with Amyotrophic Lateral Sclerosis, Is Antagonized by Riluzole

Yáñez¹,

Matías‐Guiu²,

Arranz-Tagarro³

et al. 2013

Neurodegener Dis

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In a recent study we found that cerebrospinal fluids (CSFs) from amyotrophic lateral sclerosis (ALS) patients caused 20-30% loss of cell viability in primary cultures of rat embryo motor cortex neurons. We also found that the antioxidant resveratrol protected against such damaging effects and that, surprisingly, riluzole antagonized its protecting effects. Here we have extended this study to the interactions of riluzole with 3 other recognized neuroprotective agents, namely memantine, minocycline and lithium. We found: (1) by itself riluzole exerted neurotoxic effects at concentrations of 3-30 µM; this cell damage was similar to that elicited by 30 µM glutamate and a 10% dilution of ALS/CSF; (2) memantine (0.1-30 µM), minocycline (0.03-1 µM) and lithium (1-80 µg/ml) afforded 10-30% protection against ALS/CSF-elicited neurotoxicity, and (3) at 1-10 µM, riluzole antagonized the protection afforded by the 3 agents. These results strongly support the view that at the riluzole concentrations reached in the brain of patients, the neurotoxic effects of this drug could be masking the potential neuroprotective actions of new compounds being tested in clinical trials. Therefore, in the light of the present results, the inclusion of a group of patients free of riluzole treatment may be mandatory in future clinical trials performed in ALS patients with novel neuroprotective compounds.

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“…The latter enzyme is also involved in pro-apoptotic cell signaling. Lithium is neuroprotective against cell injuries caused by glutamate excitotoxicity [24,25], b-amyloid [26][27][28], colchicine [29], growth factor withdrawal [30], irradiation [31], exposure to heat shock [32], etc. Recent studies have shown that lithium decreases Bax protein levels and increases Bcl-2/Bax ratio [7].…”

Section: Discussionmentioning

confidence: 99%

Chronic Lithium Impairs Skin Tolerance to Ischemia in Random-Pattern Skin Flap of Rats

Nezami¹,

Rahimpour²,

Sadeghi³

et al. 2011

Journal of Surgical Research

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Implication of cyclin-dependent kinase 5 in the neuroprotective properties of lithium

Cited by 35 publications

References 43 publications

Lithium: Potential Therapeutics Against Acute Brain Injuries and Chronic Neurodegenerative Diseases

Lithium: Potential Therapeutics Against Acute Brain Injuries and Chronic Neurodegenerative Diseases

The Neuroprotection Exerted by Memantine, Minocycline and Lithium, against Neurotoxicity of CSF from Patients with Amyotrophic Lateral Sclerosis, Is Antagonized by Riluzole

Chronic Lithium Impairs Skin Tolerance to Ischemia in Random-Pattern Skin Flap of Rats

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