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Mental Illness and Addictions Research Chair

Dr. Kathy Aitchison was appointed as the second Alberta Centennial Addiction and Mental Health Research Chair in 2011. She is a practicing psychiatrist with a PhD in pharmacogenetics—the study of how genes affect a person’s response to drugs. In her role as Research Chair, she provides leadership in mental health and addictions research with the overall goal of improving the mental health of Albertans.

Prior to coming to Alberta, Dr. Aitchison developed and led an Early Intervention in Psychosis Clinical Team, and co-led a large European research project on depression. She continues to be involved in the European STOP Study, a comprehensive evaluation of suicidality in children and adolescents. Dr. Aitchison has published extensively in the fields of psychopharmacology, pharmacogenetics, psychiatric genetics, and health care outcomes.

Dr. Aitchison is based out of the University of Alberta, where she is a Professor in the Department of Psychiatry and Adjunct Professor in the Department of Medical Genetics. She is Lead Psychiatrist of the Edmonton Early Psychosis Intervention Clinic, and has mentored clinical research trainees and supervised medical residents. She holds Visiting Professorships at the King’s College London Institute of Psychiatry and Northern Ontario School of Medicine, and is involved in many national and international research collaborations.

The Chair mandate may be summarized as follows: Through promoting and strengthening working relationships with service providers in Alberta Health Services zones, and with relevant community agencies and policy-makers, the Chair will lead change and support evidence-based practice. Dr. Aitchison’s research includes:

  • Investigation of the interaction between adverse childhood experiences, recent adverse life events, genetic vulnerability and exposure to cannabis in individuals with psychotic illnesses (e.g., schizophrenia and bipolar affective disorder).
  • Identification of genetic factors associated with risk of mental illness and addictions, as well as treatment response with the aim of enabling health promotion and prevention strategies such as individually tailored treatments.
  • Identification of biological and psychosocial factors and mediators involved in suicidal behaviours to help create protective strategies for young people.

Through knowledge gained in these areas, Dr. Aitchison’s research will help fulfill the program goals by promoting evidence-driven changes in addiction and mental health practice.

Read more about Dr. Aitchison's research on ResearcherID.

Research Summaries

Dr. Aitchison has numerous publications related to her research. Below are abstracts from a selection of relevant publications.

Roper, L. J., Purdon, S. E., & Aitchison, K. J. (2015). Childhood and later life stressors and psychosis. Clinical Neuropsychiatry, 12(6), 148–156.
Background: Psychosis may arise as a combination of one or more of the following risk factors: genetic vulnerability, adverse life events and trauma, and substance use.
Methods: Current theories on the origins of psychosis are discussed in this review. In particular, the effects of Adverse Childhood Experiences (ACEs) and stressful life events are investigated.
Results: ACEs have been associated with an increased risk of social and health issues later in life, including psychosis. Past research has found that stressful left events may contribute to the onset and relapse of psychotic episodes when combined with genetic and environmental risk factors. In particular, the authors suggest that vulnerability to stress may be involved in the onset of psychosis. Some research has indicated that particular ACEs and stressful life events maybe be associated with specific psychotic symptoms, but the results have been mixed.
Conclusions: The evidence demonstrates that ACEs and stressful life events contribute to the onset of psychosis, especially those that take place in the three months prior to onset.

Koola, M. M., Tsapakis, E. M., Wright, P., Smith, S., Kerwin, R. W., Nugent, K. L., & Aitchison, K. J. (2014). Association of tardive dyskinesia with variation in CYP2D6: Is there a role for active metabolites? Journal of Psychopharmacology, 28(7), 665–670.
Background: Individuals taking antipsychotic medications for a prolonged period may develop tardive dyskinesia (TD) as an adverse drug reaction; TD is an irreversible movement disorder. This study investigated the impact of CYP2D6 gene variants on TD risk.
Methods: A cross-sectional study of 70 Caucasian patients with a diagnosis of schizophrenia was conducted. The patients were from an outpatient clinic in South London, UK, and had been receiving antipsychotic treatment for at least 12 months prior to the study. Patient DNA was extracted from a blood sample and genotyped for CYP2D6 alleles*3–5, *41, as well as amplifications of the gene.
Results: Thirteen out of the 70 patients tested positive for TD. The patients with TD had a significantly longer average duration of antipsychotic treatment (15.8 years) than the patients without TD (11.1 years; p=0.04). The patients with TD also had a significantly higher likelihood of having drug-induced Parkinsonism (85%) compared to the patients without TD (42%; p=0.006). Ability to metabolize CYP2D6 was found to increase the odds of experiencing TD.
Conclusions: Increased ability to metabolize CYP2D6 based on a greater number of functional alleles was associated with the development of TD. The authors suggest this may be due to the generation of neurotoxic metabolites, which could be investigated in future research.

Tsapakis, E. M., Fernandes, C., Moran-Gates, T., Basu, A., Sugden, K., Aitchison, K. J., & Tarazi, F. I. (2014). Effects of antidepressant drug exposure on gene expression in the developing cerebral cortex. Synapse, 68(5), 209–220.
Background: Children and adolescents generally show limited responses to antidepressant treatment, even though antidepressants are considered a standard treatment for adults with major depressive disorder.
Methods: To help understand why children show limited responses to antidepressants, male rats were given either of the antidepressants fluoxetine or imipramine, or a control treatment of saline. After three weeks of treatment, total RNA was extracted from the frontal cortices of the rats, and hybridized to Affymetrix Rat Genome 230.2 microarrays. A total of 18 microarrays were analyzed based on six samples from each of the three treatment groups. Gene transcripts in response to the different antidepressants were identified, and the relative expression of each gene was determined.
Results: The rats that received either antidepressant treatment were found to have down-regulated expression of six genes, and over-expression of four genes. This demonstrates that antidepressant drugs can interfere with gene expression involved in cell signaling, survival, and protein metabolism.
Conclusions: The results suggest that antidepressants control how different genes are expressed in developing frontal cortices, and provide new information about the long-term molecular actions of such drugs.

Huezo-Diaz, P., Perroud, N., Spencer, E. P., Smith, R., Sim, S., Virding, S., Uher, R., Gunasinghe, C., Gray, J., Campbell, D., Hauser, J., Maier, W., Marusic, A., Rietschel, M., Perez, J., Giovannini, C., Mors, O., Mendlewicz, J., McGuffin, P., Farmer, A. E., Ingelman-Sundberg, M., Craig, I. W., Aitchison, K. J. (2012). CYP2C19 genotype predicts steady state escitalopram concentration in GENDEP. Journal of Psychopharmacology, 26(3), 398–407.
Background: Escitalopram, the S-enantiomer of the selective serotonin reuptake inhibitor (SSRI) citalopram has been shown to be effective in the treatment of major depressive disorder. The CYP2C19 genotype is involved in the metabolism of escitalopram.
Methods: The authors studied 196 European Caucasian patients aged 18–66 with depression who were receiving escitalopram treatment. DNA and serum concentrations of escitalopram were extracted through blood tests given at baseline, 12 weeks, and 26 weeks. The AmpliChip CYP450 Test was used to genotype the CYP2D6 and CYP2C19 variants.
Results: CYP2C19 genotypic category and steady state escitalopram concentration were significantly associated. Older subjects were found to have higher concentrations of escitalopram.
Conclusions: The authors confirmed the classification of CYP2C19*17 as an ultrarapid metabolizer allele, and demonstrated an association between CYP2C19 genotype, including the CYP2C19*17 allele, and escitalopram concentration.

Wolff, K., Tsapakis, E., Pariante, C., Kerwin, R., Forsling, M., & Aitchison, K. J. (2012). Pharmacogenetic studies of change in cortisol on Ecstasy (MDMA) consumption. Journal of Psychopharmacology, 26, 419-428.
Background: ‘Ecstasy’ (3,4-methylenedioxymethamphetamine [MDMA]) is a synthetic amphetamine analogue. This study investigates how cortisol concentration following Ecstasy consumption is affected by the cytochrome P450 enzyme CYP2D6 genotype, the catechol-O-methyl transferase (COMT) genotype, and serotonin transporter promoter genotype.
Methods: Forty-eight males who had been clubbing at least three times in the past month were recruited to give blood, urine, and breath-alcohol samples before and after going clubbing. The AmpliChip CYP450 Test was used to detect genetic variants in CYP2D6.
Results: Urine analysis revealed that 54% of participants tested positive for MDMA following clubbing. Those who tested positive for MDMA, also had a significantly higher concentration of plasma cortisol. There was also a positive association between the COMT genotype and change in cortisol of both MDMA users and the whole sample. The CYP2D6 genotype was only associated with cortisol change in MDMA users. There were no associations observed with the serotonin transporter promoter genotype.
Conclusions: There was a positive association with low CYP2D6 and low COMT activity genotypes. This suggests that regular consumption of MDMA could lead to hypothalamo-pituitary-adrenal axis dysregulation.

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