Mood Disorders (Psychology)

Low-dose tryptophan depletion in recovered depressed women induces impairments in autobiographical memory specificity

by Anneke Haddad

Haddad, A. D. M., Williams, J. M. G., McTavish, S. F. B., & Harmer, C. J. (2009, December). Low-dose tryptophan depletion in recovered depressed women induces impairments in autobiographical memory specificity.. Psychopharmacology (Berl), 207(3), 499-508.

Background: Depressed patients perform poorly on tests of autobiographical memory specificity (AMS); this may have... more Background: Depressed patients perform poorly on tests of autobiographical memory specificity (AMS); this may have negative consequences for other important cognitive abilities, delays recovery from mood episodes, and, in recovered patients, may mediate vulnerability to future episodes. Although the cognitive mechanisms underlying AMS deficits are beginning to be understood, the neurobiological mechanisms remain unclear. Serotonin is implicated in both depression and long-term memory; therefore, temporary lowering of brain serotonin function via acute tryptophan depletion (ATD) offers a means of studying the role of serotonin in autobiographical memory specificity.

Materials and methods: In this study, 24 previously depressed women underwent low-dose ATD or sham depletion and completed tests of initial and delayed memory, recollection- and familiarity-based recognition, and AMS.

Results: ATD did not differentially affect state mood. Compared with sham depletion, ATD impaired immediate recall on the Auditory Verbal Learning Test. Although ATD did not differentially impair recollection- and familiarity-based recognition, it did slow recognition of positive words. ATD also reduced autobiographical memory specificity in response to negative cue words.

Discussion: The results confirm previous findings that low-dose ATD can reinstate depression-congruent biases in cognition without causing depressive mood in vulnerable populations. The ATD-induced reduction in memory specificity suggests that serotonergic dysfunction may mediate depressive deficits in autobiographical memory; the interaction of cognitive and neurobiological vulnerability mechanisms is discussed.

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

by Mohammad Alsuwaidan

Effects of omega-3 fatty acids on cognitive performance: a meta-analysis

by Graham Mazereeuw

Graham Mazereeuw, Krista L. Lanctôt, Sarah A. Chau, Walter Swardfager, Nathan Herrmann. Neurobiol Aging. 2012. Article in Press.

Background: Higher intake of omega-3 fatty acids (n-3 FAs) is associated with a reduced risk of Alzheimer's disease... more Background: Higher intake of omega-3 fatty acids (n-3 FAs) is associated with a reduced risk of Alzheimer's disease (AD) and milder forms of cognitive impairment (e.g. cognitive impairment no dementia [CIND]); however, findings from interventional trials are inconsistent. This meta-analysis examined the neuropsychological benefit of n-3 FAs in randomized double-blind placebo-controlled studies (RCTs) including healthy, CIND, or AD subjects.

Methods: Literature was searched using Medline, Embase, PsycInfo, Cochrane Library, Allied and Complementary Medicine Database (AMED), and Cumulative Index to Nursing and Allied Health Literature (CINAHL) up to September 2011. Treatment effects were summarized across cognitive subdomains, and effect sizes were estimated using Hedge's g and random effects modeling.

Results: Ten RCTs were combined quantitatively. There was no effect of n-3 FAs on composite memory (g = 0.04 [95% CI: −0.06–0.14], N = 934/812, p = 0.452). When examined by domain, no overall benefit for immediate recall (0.04 [−0.05–0.13], N = 934/812, p = 0.358) was detected; however, an effect in CIND subjects (0.16 [0.01–0.31], N = 349/327, p = 0.034) was found. A benefit for attention and processing speed was also detected in CIND (0.30 [0.02–0.57], N = 107/86, p = 0.035), but not healthy subjects. Benefits for delayed recall, recognition memory, or working memory and executive function were not observed. Treatment did not benefit AD patients as measured by the Mini-Mental State Examination (MMSE) or Alzheimer's Disease Assessment Scale–Cognitive Subscale (ADAS–cog). No differences in adverse events (AE), dropout, or dropout due to AE between groups were observed.

Conclusions: These results suggest an effect of n-3 FAs within specific cognitive domains in CIND, but not in healthy or AD subjects.

Associations between n-3 PUFA concentrations and cognitive function after recovery from late-life depression.

by Sophia Frangou

Chiu CC, Frangou S, Chang CJ, Chiu WC, Liu HC, Sun IW, Liu SI, Lu ML, Chen CH, Huang SY, Dewey ME, Stewart R.

Am J Clin Nutr. 2012; 95: 2; 420-427

BACKGROUND: Lower concentrations of n-3 PUFAs have been reported to be associated with cognitive impairment and... more BACKGROUND: Lower concentrations of n-3 PUFAs have been reported to be associated with cognitive impairment and dementia, but also with depression-itself a potential risk factor for cognitive decline.

OBJECTIVE: The aims of this study were to investigate associations between n-3 PUFA concentrations in erythrocyte membrane or plasma and cognitive function in an at-risk sample of older people with previous major depression and to explore specificity with respect to cognitive domains.

DESIGN: A cross-sectional sample of 132 eligible participants who had recovered from major depression (mean ± SD age: 67.8 ± 6.6 y) were enrolled from outpatient psychiatric services. A series of cognitive tests and a structured questionnaire were administered. Fasting blood samples were collected for n-3 PUFA measurements.

RESULTS: Higher EPA and total n-3 PUFA concentrations and a lower ratio of arachidonic acid to EPA in erythrocyte membranes were associated with a higher cognitive composite score: independent of age and sex, but no longer significant after adjustment for education. No associations were found with plasma concentrations of any fatty acid. Considering individual cognitive tests, the strongest and most consistent correlations were found between immediate recall and concentrations of total n-3 PUFAs and α-linolenic acid (ALA) in erythrocytes, which were observed only in participants with recurrent depression.

CONCLUSIONS: Total erythrocyte n-3 PUFA concentrations are positively associated with cognitive function, particularly immediate recall, in older people with previous depression. Lower concentrations of n-3 PUFAs or ALA in erythrocyte membranes may be good predictors for cognitive impairment in older people with previous recurrent depression.

Research Letter: High-density negative ion treatment increases positive affective memory

by Charlotte Malcolm

Can We Remember Future Actions yet Forget the Last Two Minutes? Study in Transient Global Amnesia

by Mathieu Hainselin

Healing Childhood Sexual Abuse

by Daniel Keeran MSW

by Daniel Keeran, MSW, RMHC-S

The College of Mental Health Counseling presents a summary process for healing childhood sexual abuse that is... more The College of Mental Health Counseling presents a summary process for healing childhood sexual abuse that is sometimes an issue underlying mood and anxiety disorders, PTSD, marital problems, suicidality, addiction, eating disorders, borderline and histrionic personality disorders, other mental distress.

The experience of sexual abuse in childhood is one of the most sensitive kinds of trauma addressed in counseling. Those in the helping professions need clear and practical approaches to assist survivors of sexual abuse, recognizing that the healing process may be lengthy and that a single counselor may realistically only be able to help the individual partially heal the pain and effects of the abuse.

This report is adapted from the book “Effective Counseling Skills” by the author, in digital and hard copy at http://www.amazon.com/Effective-Counseling-Skills-therapeutic-statements/dp/1442177993

Healing the experience of childhood sexual abuse involves helping the client begin to disclose the experience, addressing the painful emotions associated with the abuse, understanding the affects and unhealthy decisions and beliefs related to the abuse, and then adopting healthy decisions and beliefs and caring self-talk.

Postmodern Anomic Disorder* (PAD): Understanding Gang Behavior and the London Riots

by Daniel Keeran MSW

by Daniel Keeran, MSW

The College of Mental Health Counseling presents an understanding of youth gangs, the London riots, Islamic terrorism, aboriginal suicide and other similar phenomena as possible effects of Postmodern Anomic Disorder* identified here for the first time.

If the paper does not yet appear below, you can download it here http://www.ctihalifax.com/images/Anomic_Disorder4.pdf

If you have any questions, comments, or upload difficulty, please contact collegemhc@gmail.com

The College of Mental Health Counseling presents an understanding of youth gangs, the London riots, Islamic terrorism,... more The College of Mental Health Counseling presents an understanding of youth gangs, the London riots, Islamic terrorism, aboriginal suicide and other similar phenomena as possible effects of Postmodern Anomic Disorder* identified here for the first time.

If you have any questions or comments please contact collegemhc@gmail.com

5-HT Modulation by Acute Tryptophan Depletion of Human Instrumental Contingency Judgements

by Rachel Msetfi

Amygdala to hippocampal volume ratio is associated with negative memory bias in healthy subjects

by Lotte Gerritsen

accepted for publication in Psychological Medicine

Background
Negative memory bias is thought to be one of the main cognitive risk and maintenance factors for... more Background
Negative memory bias is thought to be one of the main cognitive risk and maintenance factors for depression, but its neural substrates are largely unknown. Here we studied whether memory bias is related to amygdala and hippocampal volume, two structures that are critical for emotional memory processes and that show consistent volume alterations in depression.
Methods
Structural magnetic resonance imaging was carried out in 272 healthy participants (62% female, 18-50 yrs old). All images were acquired on 1.5 T Siemens MRI scanners. Automatic segmentation of amygdala and hippocampus was performed using the FIRST module of FSL. Negative memory bias was assessed by the self-referent encoding/evaluation test.
Results
Negative memory bias was associated with larger amygdala (p=0.042) and smaller hippocampal volume (p=0.029). In additional analyses we found that compared to the associations found with hippocampus and amygdala volume separately a stronger association was found between negative memory bias and the ratio of amygdala to hippocampus volume (p = 0.021).
Conclusions
In non-depressed subjects we found that larger amygdala and smaller hippocampal volumes are associated with negative memory bias. This suggests that an increased amygdala/hippocampus volume ratio plays a role in cognitive vulnerability often seen in individuals with high risk for depression and that these structural brain differences may antedate the onset of depression.

The effect of bipolar I disorder and major depressive disorder on workforce function

by Mohammad Alsuwaidan

Mood and Anxiety Disorders Rounds™

by Mohammad Alsuwaidan

Bipolar disorder and metabolic syndrome: An international perspective

by Mohammad Alsuwaidan

Exercise and Bipolar Disorder: A Review of Neurobiological Mediators

by Mohammad Alsuwaidan

Metabolic Syndrome and Major Depressive Disorder: Co-Occurrence and Pathophysiologic Overlap

by Mohammad Alsuwaidan

Aerobic physical exercise as a possible treatment for neurocognitive dysfunction in bipolar disorder.

by Mohammad Alsuwaidan

Modelling Facets of Mania-New Directions Related to the Notion of Endophenotypes

by Haim Einat

J Psychopharmacol. 2006 Sep;20(5):714-22.

The lack of appropriate animal models is a major limitation in research of bipolar disorder (BPD): at this time there... more The lack of appropriate animal models is a major limitation in research of bipolar disorder (BPD): at this time there are very few models for this devastating disease. Whereas limited attempts have been made to develop comprehensive models for BPD, the new notion of endophenotypes encourages us to explore the possibility of developing separate models for separate facets of the disorder. Since more models are available for depression, there is a dire need for models for mania that will be relatively easy and simple to induce and test and will therefore be practical for purposes of screening possible new drugs or mutant mice that are developed based on novel molecular theories. Such models may already be tentatively available as they were developed in the context of other disorders, but there is a need to validate them for mania. The present paper proposes such models for most of the facets of mania including: increased energy, activity or restlessness; extreme irritability; reduced sleep; provocative, intrusive or aggressive behaviour; increased sexual drive; abuse of drugs; distractibility, reduced ability to concentrate; and unrealistic beliefs in one's abilities and powers resulting in poor judgement. Validating these models may demand a major research effort but it may be worthy as validated models for the different facets of mania could then be used efficiently and may be utilized to construct a standard battery of tests that can serve to explore the various components of manic-like behaviour in rodents.

New approaches to modeling bipolar disorder – from face to construct validity.

by Haim Einat

Einat H, Belmaker RH and Manji HK
Psychopharmacology Bulletin 37(1): 47-63.

Increased Anxiety-Like Behaviors and Mitochondrial Dysfunction In Mice With Targeted Mutation of the Bcl-2 Gene: Further Support for the Involvement of Mitochondrial …

by Haim Einat

Cellular Plasticity Cascades: Genes-to-Behavior Pathways In Animal Models of Bipolar Disorder

by Haim Einat

Haim Einat & Husseini K Manji
BIOL PSYCHIATRY 2006;59:1160–1171

Background: Despite extensive research, the molecular/cellular underpinnings of bipolar disorder (BD) remain to be... more Background: Despite extensive research, the molecular/cellular underpinnings of bipolar disorder (BD) remain to be fully elucidated. Recent data has demonstrated that mood stabilizers exert major effects on signaling that regulate cellular plasticity; however, a direct extrapolation to mechanisms of disease demands proof that manipulation of candidate genes, proteins, or pathways result in relevant
behavioral changes. Methods: We critique and evaluate the behavioral changes induced by manipulation of cellular plasticity cascades implicated in BD.
Results: Not surprisingly, the behavioral data suggest that several important signaling molecules might play important roles in mediating facets of the complex symptomatology of BD. Notably, the protein kinase C and extracellular signal-regulated kinase cascades might play important roles in the antimanic effects of mood stabilizers, whereas glycogen synthase kinase (GSK)-3 might mediate facets of lithium’s antimanic/antidepressant actions. Glucocorticoid receptor (GR) modulation also seems to be capable to inducing affective-like changes observed in mood disorders. And Bcl-2, amino-3-hydroxy-5-methylisoxazole-4-propionic acid
receptors, and inositol homeostasis represent important pharmacological targets for mood stabilizers, but additional behavioral research is needed to more fully delineate their behavioral effects.
Conclusions: Behavioral data support the notion that regulation of cellular plasticity is involved in affective-like behavioral changes observed in BD. These findings are leading to the development of novel therapeutics for this devastating illness.