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A glycogen synthase kinase 3-β promoter gene single nucleotide polymorphism is associated with age at onset and response to total sleep deprivation in bipolar depression
Abstract
The molecular mechanisms driving the biological clock in the suprachiasmatic nucleus of the hypothalamus may play a role in mood disorders. A single nucleotide polymorphism (SNP) (-50T/C) falling into the effective promoter region (nt -171 to +29) of the gene coding for glycogen synthase kinase 3-beta (GSK3-beta) has been linked with different age at onset of bipolar illness. GSK3-beta codes for an enzyme which is a target for the action of lithium and valproic acid, and the inhibition of which causes antidepressant-like behaviors in a preclinical model. We studied the effect of this polymorphism on the acute response to total sleep deprivation of 60 depressed bipolar type I inpatients. Homozygotes for the mutant allele of GSK3-beta promoter (-50T/C) SNP showed a later onset of bipolar illness, and better acute effects of TSD treatment on perceived mood (as rated on VAS). Overall, these observations suggest a protective role for this genotype in respect to bipolar illness. Results warrant interest for the variants of genes pertaining to the molecular clock as possible endophenotypes of bipolar disorder, and for GSK3-beta as a target of a new class of antidepressant drugs, but caution ought to be taken in interpreting these preliminary results and future replication studies must be awaited because of the low frequency of the GSK3-beta*C/C genotype in the studied populations.
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“other studies failed to show a general association between these SNPs and BPD”
From Circadian genes, rhythms and the biology of mood disorders (2007) · cites this paper as Benedetti et al., 2004
In the citing paper
“one of these SNPs (−50 T to C) is linked to a later age of onset of BPD and a greater response to total sleep deprivation (TSD) and long-term lithium treatment (Benedetti et al., 2004; Benedetti et al., 2005).”
From Circadian genes, rhythms and the biology of mood disorders (2007) · cites this paper as Benedetti et al., 2004
In the citing paper
“one of these SNPs (−50 T to C) is linked to a later age of onset of BPD and a greater response to total sleep deprivation (TSD) and long-term lithium treatment (Benedetti et al., 2004; Benedetti et al., 2005).”
From Circadian genes, rhythms and the biology of mood disorders (2007) · cites this paper as Benedetti et al., 2004
In the citing paper
“one of these SNPs (−50 T to C) is linked to a later age of onset of BPD and a greater response to total sleep deprivation (TSD) and long-term lithium treatment (Benedetti et al., 2004; Benedetti et al., 2005).”
From Circadian genes, rhythms and the biology of mood disorders (2007) · cites this paper as Benedetti et al., 2004
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“PKC also causes the phosphorylate and inactivate GSK-3β in vitro [39, 40], as well as regulati ng of GSK-3 during signaling routs the activity of this critical enzyme.”
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“Disordered GSK-3 β signaling pathways underlie the pathogenesis of bipolar disorder (BD) [56].”
Metadata
- Authors
- Benedetti, F., Serretti, A., Colombo, C., Lorenzi, C., Tubazio, V., & Smeraldi, E.
- Affiliations
- Vita-Salute San Raffaele University (IT)
- IRCCS Ospedale San Raffaele (IT)
- Corresponding author
- Benedetti, Francesco
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2004-09
- Volume
- 368
- Issue
- 2
- Pages
- 123-126
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2080758948
- Cited by
- 195
- References
- 26
- Citations by year
- 2026: 3 · 2025: 2 · 2023: 2 · 2022: 4 · 2021: 27 · 2020: 6 · 2019: 3 · 2018: 6 · 2017: 6 · 2016: 8 · 2015: 13 · 2014: 11 · 2013: 9 · 2012: 15
- FWCI
- 5.01
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- Archivio Istituzionale della Ricerca - Università Vita-Salute San Raffaele (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Bipolar Disorder and Treatment
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Keywords
- glycogen synthase kinase-3β, single nucleotide polymorphisms, total sleep deprivation, bipolar depression, bipolar I disorder, age of onset, genetic susceptibility, circadian clock, suprachiasmatic nucleus, mood disorders, antidepressant targets, endophenotypes
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Adult, Alleles, Analysis of Variance, Bipolar Disorder, DNA Mutational Analysis, Female, Genotype, Humans, Male, Middle Aged, Mutation, Promoter Regions, Genetic, Sleep Deprivation, Age of Onset, Genetic Predisposition to Disease, Reverse Transcriptase Polymerase Chain Reaction, Polymorphism, Single Nucleotide, Glycogen Synthase Kinase 3
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