Associate Professor Tom Weickert
TEAM LEADER PROFILE
Research Fellow, NeuRA
Associate Professor, School of Psychiatry, UNSW
+61 2 9399 1730
Assoc Prof Thomas Weickert received a BA in Biology from Kean University, USA and while at the Graduate School of the City University of New York (CUNY) where his studies focused on Cognition, he received an MA, an MPhil, and a PhD in Psychology. He was an Adjunct Lecturer in Psychology at Hunter College. He has received several undergraduate and graduate level academic and research awards. His dissertation work on memory deficits in healthy ageing and Alzheimer’s disease was conducted at the New York University Medical Center in Manhattan where he also worked as an assistant research scientist. He received an Intramural Research Training Award Fellowship to study cognitive deficits in schizophrenia at the National Institute of Mental Health in Bethesda, MD, USA. His research has resulted in over 45 peer-reviewed publications, which have over 1800 citations and appear in well-respected scientific journals. His first publication alone has generated over 300 citations. He is a co-author of chapters in two Psychiatry textbooks. He has been a research mentor to well over 20 students. He is a member of many scientific organisations. He is an Associate Editor of Frontiers in Psychiatry and a reviewer of grant applications and manuscripts submitted to many scientific journals. He has presented his work at many national and international scientific meetings.
Projects Associate Professor Tom Weickert is currently involved with
CURRENT PROJECTS
Blood biomarkers in melancholic and non-melancholic subtypes of depression study
A study of men and women between 18 to 70 years of age with a diagnosis of either melancholic or non-melancholic depression to research the extent to which blood biomarkers may be elevated in melancholic and non-melancholic subtypes of depression.
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Blood biomarkers in melancholic and non-melancholic subtypes of depression study
GOOGLE SCHOLAR
RESEARCH TEAM
DR DANIEL PELLEN Research Officer
DR CLIVE STANTON Visiting Research Officer
RUTH WELLS Visiting Research Assistant
HINA SALIMUDDIN Visiting Student : h.salimuddin@neura.edu.au
PUBLICATIONS
Rethinking schizophrenia in the context of normal neurodevelopment.
Catts VS, Fung SJ, Long LE, Joshi D, Vercammen A, Allen KM, Fillman SG, Rothmond DA, Sinclair D, Tiwari Y, Tsai SY, Weickert TW, Shannon Weickert C
The schizophrenia brain is differentiated from the normal brain by subtle changes, with significant overlap in measures between normal and disease states. For the past 25 years, schizophrenia has increasingly been considered a neurodevelopmental disorder. This frame of reference challenges biological researchers to consider how pathological changes identified in adult brain tissue can be accounted for by aberrant developmental processes occurring during fetal, childhood, or adolescent periods. To place schizophrenia neuropathology in a neurodevelopmental context requires solid, scrutinized evidence of changes occurring during normal development of the human brain, particularly in the cortex; however, too often data on normative developmental change are selectively referenced. This paper focuses on the development of the prefrontal cortex and charts major molecular, cellular, and behavioral events on a similar time line. We first consider the time at which human cognitive abilities such as selective attention, working memory, and inhibitory control mature, emphasizing that attainment of full adult potential is a process requiring decades. We review the timing of neurogenesis, neuronal migration, white matter changes (myelination), and synapse development. We consider how molecular changes in neurotransmitter signaling pathways are altered throughout life and how they may be concomitant with cellular and cognitive changes. We end with a consideration of how the response to drugs of abuse changes with age. We conclude that the concepts around the timing of cortical neuronal migration, interneuron maturation, and synaptic regression in humans may need revision and include greater emphasis on the protracted and dynamic changes occurring in adolescence. Updating our current understanding of post-natal neurodevelopment should aid researchers in interpreting gray matter changes and derailed neurodevelopmental processes that could underlie emergence of psychosis.
Considering the role of adolescent sex steroids in schizophrenia.
Owens SJ, Murphy CE, Purves-Tyson TD, Weickert TW, Shannon Weickert C
Schizophrenia is a disabling illness that is typically first diagnosed during late adolescence to early adulthood, has an unremitting course, and is often treatment resistance. Many clinical aspects of the illness suggest that sex steroid-nervous system interactions may contribute to the onset and course of symptoms and the cognitive impairment displayed by men and women with schizophrenia. Here, we discuss the actions of estrogen and testosterone on the brain during adolescent development and in schizophrenia from the perspective of experimental studies in animals, human post-mortem studies, magnetic resonance imaging studies in living humans, and clinical trials of sex steroid based treatments. We present evidence of potential beneficial, as well as detrimental, effects of both testosterone and estrogen. We provide a rationale for the necessity to further elucidate sex steroid mechanisms of action at different ages, genders and brain regions to more fully understand the role of testosterone and estrogen in the pathophysiology of schizophrenia. The weight of the evidence suggests that sex steroid hormones influence mammalian brain function, including both cognition and emotion and that pharmaceutical agents aimed at sex steroid receptors appear to provide a novel treatment avenue to reduce symptoms and improve cognition in men and women with schizophrenia. This article is protected by copyright. All rights reserved.
BDNF val66met genotype and schizotypal personality traits interact to influence probabilistic association learning.
Skilleter AJ, Weickert CS, Moustafa AA, Gendy R, Chan M, Arifin N, Mitchell PB, Weickert TW
The brain derived neurotrophic factor (BDNF) val66met polymorphism rs6265 influences learning and may represent a risk factor for schizophrenia. Healthy people with high schizotypal personality traits display cognitive deficits that are similar to but not as severe as those observed in schizophrenia and they can be studied without confounds of antipsychotics or chronic illness. How genetic variation in BDNF may impact learning in individuals falling along the schizophrenia spectrum is unknown. We predicted that schizotypal personality traits would influence learning and that schizotypal personality-based differences in learning would vary depending on the BDNF val66met genotype. Eighty-nine healthy adults completed the Schizotypal Personality Questionnaire (SPQ) and a probabilistic association learning test. Blood samples were genotyped for the BDNF val66met polymorphism. An ANOVA was performed with BDNF genotype (val homozygotes and met-carriers) and SPQ score (high/low) as grouping variables and probabilistic association learning as the dependent variable. Participants with low SPQ scores (fewer schizotypal personality traits) showed significantly better learning than those with high SPQ scores. BDNF met-carriers displaying few schizotypal personality traits performed best, whereas BDNF met-carriers displaying high schizotypal personality traits performed worst. Thus, the BDNF val66met polymorphism appears to influence probabilistic association learning differently depending on the extent of schizotypal personality traits displayed.