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Sent on Thursday, 2008 Nov 06.
Search bipolar disorder
Click on the following url to view complete results in pubmed. (Results may change over time.)
http://www.ncbi.nlm.nih.gov/entrez/cubby.fcgi?call=0LWWFdz-pibcTNvh80oC7qiTcQzBjxeZF8ugYlIIY2iXLT8_8vhl11DrOtAcBeJ&WebCubbyUser=0D_BjdkVNOeoTr8GNEVjS5CA%40990E5B71912EEF91_0019SID
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==================== Entrez pubmed Results ======================
Items 1 - 5 of 26
1: Sleep Breath. 2008 Nov 4; [Epub ahead of print]
Sleep in bipolar patients.
Giglio LM, Andreazza AC, Andersen M, Cereser KM, Walz JC, Sterz L, Kapczinski F.
Bipolar Disorders Program-Centro de Pesquisas, Hospital de Clinicas de Porto
Alegre, Rua Ramiro Barcelos, 2350, 90035-003, Porto Alegre, RS, Brazil,
larriany@terra.com.br.
BACKGROUND: Sleep disturbance has been described in bipolar disorder (BPD).
Specific complaints may include frequent nighttime awakenings, poor quality of
sleep, reduction in total sleep time, and nightmares. Most patients with BPD
also report insomnia when in depression, but a significant percentage of
patients report hypersomnia symptoms with prolonged nighttime sleep, difficulty
in wakening, and excessive daytime sleepiness. OBJECTIVES: The present study
aims to investigate whether bipolar patients with sleep disorders presented
impairment in quality of life, disability, and global function. METHODS: One
hundred ninety bipolar patients type-I diagnosed by application of Structured
Clinician Interview for DSM-IV Disorders (SCID), were distributed in two groups
based on absence or presence of sleep disorders. Quality of life, disability,
and global dysfunction were evaluated using the Health Organization's Quality of
Life instrument (WHOQOL-Brief), the Sheehan Disability Scale, and the Global
Assessment of Functioning (GAF), respectively. RESULTS: Sleep complaints have
negative influence on general quality of life, observed by decreased scores in
WHOQOL and GAF domains and increased Sheehan scores, indicating the importance
of maintenance of normal sleep in bipolar patients. CONCLUSION: Our results
suggest that sleep complains impair quality of life and global function.
Collectively, further studies are warranted to investigate the impairment of
sleep disturbance on others neurotrophic factors and neurochemical pathways.
PMID: 18982372 [PubMed - as supplied by publisher]
2: J Neural Transm. 2008 Nov 4; [Epub ahead of print]
A functional dopamine-beta-hydroxylase gene promoter polymorphism is associated
with impulsive personality styles, but not with affective disorders.
Hess C, Reif A, Strobel A, Boreatti-Hummer A, Heine M, Lesch KP, Jacob CP.
Department of Psychiatry and Psychotherapy, Clinical and Molecular
Psychobiology, University of Wuerzburg, Fuechsleinstrasse 15, 97080, Wuerzburg,
Germany.
Dopamine-beta-hydroxylase (DbetaH) catalyzes the conversion of dopamine to
norepinephrine in central noradrenergic and adrenergic neurons and thus is
critically involved in the biosynthesis of catecholamines. There are equivocal
findings concerning the question whether or not DssH activity levels are altered
in affective disorders or in subtypes of affective disorders. Moreover,
information about the role of dopamine beta-hydroxylase (DBH) genotype, which
explains a large part of the variance of enzymatic activity, in affective
disorders and personality dimensions is limited. To resolve these
inconsistencies, association tests were performed using four independent
samples, healthy volunteers (N = 387), patients with affective disorders (N =
182), adult attention deficit hyperactivity disorder (ADHD) patients (N = 407),
and patients with personality disorders (N = 637). In the latter two samples,
the revised NEO personality inventory (NEO-PI-R) was administered. All
participants were genotyped for a putatively functional single nucleotide
polymorphism (C-1021T, rs1611115). No differences in DBH C-1021T genotype
distribution were observed between patients with affective disorders and healthy
control subjects. Also when the patient sample was divided into uni- and bipolar
patients versus controls, no significant differences emerged. Furthermore, no
clear-cut association was detected between the TT genotype and personality
disorder clusters while there was a significant association with adult ADHD.
However, personality disorder patients carrying the DBH TT genotype exhibited
higher neuroticism and novelty seeking scores as compared to individuals with
the CC or CT genotype. Analyses on the level of the neuroticism and novelty
seeking subscales revealed that the DBH TT genotype was primarily associated
with personality features related to impulsiveness and aggressive hostility.
Also adult ADHD patients carrying the homozygous TT genotypes displayed by
significantly increased neuroticism scores; when both personality disorder and
adult ADHD patient were analyzed together, TT carriers also displayed by
significantly lower conscientiousness levels. Our results thus do not implicate
the DBH C-1021T polymorphism in the pathophysiology of depressive disorders or
personality disorders, yet homozygosity at this locus appears to increase the
risk towards personality traits related to impulsiveness, aggression and related
disease states, namely adult ADHD. These data argue for a dimensional rather
than categorical effect of genetic variance in DBH activity; accordingly, the
inconsistency of previous findings concerning DbetaH levels in affective
disorders might be caused by the underlying association of the TT genotype at
DBH-1021 with impulsive personality traits.
PMID: 18982239 [PubMed - as supplied by publisher]
3: J Psychiatry Neurosci. 2008 Nov;33(6):531-40.
A comparison of affected and unaffected relatives of patients with bipolar
disorder using proton magnetic resonance spectroscopy.
Hajek T, Bernier D, Slaney C, Propper L, Schmidt M, Carrey N, MacQueen G, Duffy
A, Alda M.
Department of Psychiatry, Dalhousie University, Halifax, NS.
OBJECTIVE: Bipolar disorders have a strong genetic underpinning. Little is known
about biological predispositions that convey vulnerability for the illness. We
searched for biological vulnerability markers using proton magnetic resonance
spectroscopy (MRS) in both affected and unaffected participants at high genetic
risk for bipolar disorder. METHODS: We recruited high-risk participants aged
15-30 years from families in which multiple members were affected with bipolar
disorder. Our primary sample included 14 affected and 15 unaffected relatives of
probands with bipolar I disorder. Our extended sample comprised 19 affected and
21 unaffected participants with a family history of either bipolar I or bipolar
II disorders. We matched both samples by age and sex with 31 control
participants without a personal or family history of psychiatric disorders. We
performed single voxel proton MRS at 1.5 T in bilateral dorsal and ventral
medial prefrontal cortices with correction for grey matter proportion. RESULTS:
We found comparable levels of choline, creatine, myo-inositol and
N-acetylaspartate among the groups in both samples. There were no differences
between regions of the medial prefrontal cortex or between hemispheres for any
of the metabolites in any of the samples. The exclusion of 5 participants taking
medication did not change our results. CONCLUSION: Neurochemical changes in the
medial prefrontal cortex that are measurable using proton MRS do not appear to
be antecedent to the onset of mood disorders in genetically susceptible
individuals.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 18982176 [PubMed - in process]
4: J Psychiatry Neurosci. 2008 Nov;33(6):516-24.
Effects of mood stabilizers on DNA damage in an animal model of mania.
Andreazza AC, Kauer-Sant'Anna M, Frey BN, Stertz L, Zanotto C, Ribeiro L,
Giasson K, Valvassori SS, Reus GZ, Salvador M, Quevedo J, Goncalves CA,
Kapczinski F.
Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Brazil.
OBJECTIVE: Recent studies have suggested that oxidative stress and DNA damage
may play a role in the pathophysiology of bipolar disorder (BD). We investigated
the effects of the mood stabilizers lithium and valproate on amphetamine-induced
DNA damage in an animal model of mania and their correlation with oxidative
stress markers. METHODS: In the first experiment (reversal model), we treated
adult male Wistar rats with D-amphetamine (AMPH) or saline for 14 days; between
the 8th and 14th days, rats also received lithium, valproate or saline. In the
second experiment (prevention model), rats received either lithium, valproate or
saline for 14 days; between the 8th and 14th days, we added AMPH or saline. We
evaluated DNA damage using single-cell gel electrophoresis (comet assay), and we
assessed the mutagenic potential using the micronucleus test. We assessed
oxidative stress levels by lipid peroxidation levels (TBARS) and antioxidant
enzyme activities (superoxide dismutase and catalase). We assessed DNA damage
and oxidative stress markers in blood/plasma and hippocampal samples. We
evaluated mutagenesis in fresh lymphocytes. RESULTS: In both models, we found
that AMPH increased peripheral and hippocampal DNA damage. The index of DNA
damage correlated positively with lipid peroxidation, whereas lithium and
valproate were able to modulate the oxidative balance and prevent recent damage
to the DNA. However, lithium and valproate were not able to prevent micronucleus
formation. CONCLUSION: Our results support the notion that lithium and valproate
exert central and peripheral antioxidant-like properties. In addition, the
protection to the integrity of DNA conferred by lithium seems to be limited to
transient DNA damage and does not alter micronuclei formation.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 18982174 [PubMed - in process]
5: Mol Psychiatry. 2008 Nov 4; [Epub ahead of print]
Chronic imipramine but not bupropion increases arachidonic acid signaling in rat
brain: is this related to 'switching' in bipolar disorder?
Lee HJ, Rao JS, Chang L, Rapoport SI, Kim HW.
1Brain Physiology and Metabolism Section, National Institute on Aging, National
Institutes of Health, Bethesda, MD, USA.
Agents effective against mania in bipolar disorder are reported to decrease
turnover of arachidonic acid (AA) in phospholipids and expression of
calcium-dependent AA-selective cytosolic phospholipase A(2) (cPLA(2)) in rat
brain. In contrast, fluoxetine, an antidepressant that is reported to switch
bipolar depressed patients to mania, increases cPLA(2) expression and AA
turnover in rat brain. We therefore hypothesized that antidepressants that
increase switching to mania generally increase cPLA(2) and AA turnover in brain.
To test this hypothesis, adult male CDF-344 rats were administered imipramine
and bupropion, with reported high and low switching rates, respectively, at
daily doses of 10 and 30 mg kg(-1) i.p., respectively, or i.p. saline (control)
for 21 days. Frontal cortex expression of different PLA(2) enzymes and AA
turnover rates in brain when the rats were unanesthetized were measured.
Compared with chronic saline, chronic imipramine but not bupropion significantly
increased cortex cPLA(2) mRNA activity, protein and phosphorylation, expression
of the cPLA(2) transcription factor, activator protein-2alpha (AP-2alpha) and AA
turnover in phospholipids. Protein levels of secretory phospholipase A(2),
calcium-independent phospholipase A(2), cyclooxygenase (COX)-1 and COX-2 were
unchanged, and prostaglandin E(2) was unaffected. These results, taken with
prior data on chronic fluoxetine in rats, suggest that antidepressants that
increase the switching tendency of bipolar depressed patients to mania do so by
increasing AA recycling and metabolism in brain. Mania in bipolar disorder thus
may involve upregulated brain AA metabolism.Molecular Psychiatry advance online
publication, 4 November 2008; doi:10.1038/mp.2008.117.
PMID: 18982003 [PubMed - as supplied by publisher]