Relationship between antidepressants and IGF-1 system in the brain: Possible role in cognition

Grunbaum-Novak, Nurit; Taler, Michal; Gil-Ad, Irit; Weizman, Abraham; Cohen, Hagit; Weizman, Ronit

doi:10.1016/j.euroneuro.2007.08.004

Cited by 35 publications

(18 citation statements)

References 35 publications

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“…Fluoxetine and ECT can induce the genesis of bipotential glial progenitors and OPCs in animal brains (Hitoshi et al, 2007;Wennstrom et al, 2004). Fluoxetine has also shown an ability to promote the development of oligodendrocytes by increasing the expressions of insulin-like growth factor I (IGF-I) and its receptor in rat brains (Grunbaum-Novak et al, 2008). These findings suggest a possible outcome of antidepressant treatment is to increase the available functioning oligodendrocytes in the brains of patients with MDD by increasing the genesis or development of OPCs.…”

Section: Antidepressant Treatment May Increase Functioning Of Oligodementioning

confidence: 90%

“…Expression of IGF-I could also be increased by modulating cAMP levels (Palacios et al, 2005). A recent study has shown that chronic treatment of fluoxetine increases the levels of both IGF-1 mRNA and IGF-I receptors in the frontal cortex but not the hippocampus in rat brains (Grunbaum-Novak et al, 2008). Furthermore, intracerebroventricular administration of IGF-I has shown antidepressant-like behavioral effects with increased serotonin transmissions in rodent models (Hoshaw et al, 2008).…”

Section: Antidepressant Treatment May Increase Functioning Of Oligodementioning

confidence: 99%

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Hyperforin promotes mitochondrial function and development of oligodendrocytes

Wang

Zhang

et al. 2011

Journal of Neurochemistry

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Major depressive disorder is a common severe psychiatric disorder with unknown etiology. Recent studies show that the loss and malfunction of oligodendrocytes are closely related to the neuropathological changes in depression, which can be reversed by antidepressant treatment. St. John's wort is an effective and safe herbal treatment for depression in several clinical trials. However, the underlying mechanism of its therapeutic effects is unclear. In this study, we evaluated the effects of hyperforin, a iii ACKNOWLEDGEMENTS

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Section: Antidepressant Treatment May Increase Functioning Of Oligodementioning

confidence: 90%

Section: Antidepressant Treatment May Increase Functioning Of Oligodementioning

confidence: 99%

Hyperforin promotes mitochondrial function and development of oligodendrocytes

Wang

Zhang

et al. 2011

Journal of Neurochemistry

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“…In adult rats, Grunbaum-Novak et al (18) showed that chronic (3 times /week × 3 weeks) oral administration of fluoxetine increased IGF-I mRNA and IGF-I receptor protein levels in the frontal cortex, while decreasing those levels in the hippocampus.…”

Section: Up-regulation Of Igf-i By Antidepressant Drugs: Neurogenesismentioning

confidence: 99%

“…Lithium up-regulates IGF-II expression (19). Antidepressants up-regulate expression of IGF-I (16,18) and BDNF (17). IGF-I up-regulates BDNF expression (17,20) and its receptor TrkB level (21).…”

mentioning

confidence: 99%

Lithium and Neuropsychiatric Therapeutics: Neuroplasticity via Glycogen Synthase Kinase-3β, β-Catenin, and Neurotrophin Cascades

Wada

2009

J Pharmacol Sci

125

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Abstract. Mood disorders are not merely attributed to the functional defect of neurotransmission, but also are due to the structural impairment of neuroplasticity. Chronic stress decreases neurotrophin levels, precipitating or exacerbating depression; conversely, antidepressants increase expression of various neurotrophins (e.g., brain-derived neurotrophic factor and vascular endothelial growth factor), thereby blocking or reversing structural and functional pathologies via promoting neurogenesis. Since the worldwide approval of lithium therapy in 1970, lithium has been used for its anti-manic, antidepressant, and anti-suicidal effects, yet the therapeutic mechanisms at the cellular level remain not-fully defined. During the last five years, multiple lines of evidence have shown that the mood stabilization and neurogenesis by lithium are due to the lithium-induced inhibition of glycogen synthase kinase-3β (GSK-3β), allowing accumulation of β-catenin and β-catenin-dependent gene transcriptional events. Altered levels of GSK-3β and β-catenin are associated with various neuropsychiatric and neurodegenerative diseases, while various classical neuropsychiatric drugs inhibit GSK-3β and up-regulate β-catenin expression. In addition, evidence has emerged that insulin-like growth factor-I enhances antidepression, antianxiety, memory, neurogenesis, and angiogenesis; antidepressants up-regulate expression of insulin-like growth factor-I, while insulin-like growth factor-I up-regulates brain-derived neurotrophic factor expression and its receptor TrkB level, as well as brain-derived neurotrophic factor-induced synaptic protein levels. More importantly, physical exercise and healthy diet raise transport of peripheral circulating insulin-like growth factor I into the brain, reinforcing the expression of neurotrophins (e.g., brain-derived neurotrophic factor) and the strength of cell survival signalings (e.g., phosphoinositide 3-kinase / Akt / GSK-3β pathway). This review will focus on the rapidly advancing new trends in the last five years about lithium, GSK-3β/ β-catenin, and neurotrophin cascades.

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“…In line with this, compounds that affect mood and plasticity after brain injuries also affect local IGF1. Specifically, serotonin reuptake inhibitors, which affects local brain IGF1 levels in experimental animals (1), also improve stroke outcome in humans (2). Furthermore, circulating serum IGF1 (s-IGF1) is associated with better recovery after ischemic stroke (IS) (3,4).…”

Section: Introductionmentioning

confidence: 99%

Genetic variation at the IGF1 locus shows association with post-stroke outcome and to circulating IGF1

Åberg

Olsson

Åberg

et al. 2013

European Journal of Endocrinology

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Objective: In humans, serum IGF1 (s-IGF1) is associated with outcome after ischemic stroke (IS). Therefore variation at the IGF1 locus could also associate with both IS and s-IGF1. We investigated whether genetic variation at the IGF1 locus is associated with i) s-IGF1, ii) IS occurrence, iii) IS severity, and iv) post-stroke outcome. Design/methods: Patients (nZ844; 66% males, mean age 56 years) and community controls (nZ668) were included from the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS). Post-stroke outcome was evaluated with the modified Rankin Scale at 3 and 24 months after index stroke, and baseline stroke severity with the Scandinavian Stroke Scale. s-IGF1 was determined in patients and after random selection in 40 of the controls. Results: Eleven single nucleotide polymorphisms (SNPs) were selected in the IGF1 gene. In healthy controls the major allele of rs7136446 was associated with higher s-IGF1, whereas in patients no such association was found. No SNP was associated with IS, nor with stroke severity. After multivariate correction for presence of diabetes, smoking, and hypertension, the major allele of rs7136446 was associated with favorable functional outcome 24-months post-stroke (odds ratio 1.46; 95% CI 1.09-1.96). Conclusion: Variation in rs7136446 of the IGF1 gene associates with post-stroke outcome in relatively young IS patients. Also, rs7136446 associates with s-IGF1 in controls but not in IS, which indicates that IS perturbs a normal genetic impact on s-IGF1 levels.

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Relationship between antidepressants and IGF-1 system in the brain: Possible role in cognition

Cited by 35 publications

References 35 publications

Hyperforin promotes mitochondrial function and development of oligodendrocytes

Hyperforin promotes mitochondrial function and development of oligodendrocytes

Lithium and Neuropsychiatric Therapeutics: Neuroplasticity via Glycogen Synthase Kinase-3β, β-Catenin, and Neurotrophin Cascades

Genetic variation at the IGF1 locus shows association with post-stroke outcome and to circulating IGF1

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