A Look into Neuroscience

October 16, 2019 7:00 pm

Turhan Canli, Ph.D

Professor, Integrative Neuroscience

Research Interests:

  1. One of my core research interests addresses this central question: What are the biological mechanisms that shape (and are shaped by!) individual differences in emotion, personality, and social cognitions? How do these mechanisms explain links to well-being and health? Past work included studies of sex differences in emotional memory [1], personality [2], genetic polymorphisms [3] and gene-by-environment interactions [4]. Our current work focuses on the role of aging, social stress, loneliness, and “Purpose in Life”. My lab has equal footing in psychology, neuroscience, and molecular biology, spanning behavioral, neural, and molecular levels of analysis. Our work is mostly conducted in humans and in postmortem brain tissue from donors with extensively documented behavioral phenotypes, but also in cell culture and soon in neurogenetically manipulated rats.
  2. A second research interest concerns the etiology of depression. In a paper [5] that has been accessed more than 40,000 times since November 2014 and a TEDx talk that has been viewed 100,000 times since December 2014 [6], I have argued that brain changes associated with Major Depressive Disorder (MDD) may be caused by some form of pathogen, which could be viral, bacterial, or parasitic. I also presented an expanded exposition in a book I edited for Oxford University Press [7].
  3. A third area of interest concerns Neuroethics. I am a co-founder of the International Neuroethics Society (www.neuroethicssociety.org), which addresses the ethical, legal, and social implications (ELSI) of real-world applications of neuroscience. For example, I have published on the use of neurotechnologies in the context of National Security [8] and the emerging field of neurogenethics [9], in which neuroscience and neuroethics converge with genomics, creating a novel set of ELSI questions.

Current Research:

  1. Anxiety: What regulates gene expression in the human amygdala as a function of trait anxiety? We use a multi-pronged approach to discover novel genes associated with trait anxiety. Through a collaboration with Dr. David Bennett, Director of the Rush Alzheimer’s Disease Center, and his Memory and Aging Project (MAP), we study genome-wide RNA and global protein expression of the postmortem lateral amygdala from donors with known anxiety phenotypes. We cross-reference candidate genes with an existing genome-wide-association (GWA) database from a general population and another database from a clinical population. We conduct MRI studies to examine the structural and functional associations of novel DNA variations. We run social stress studies to study associations of these genes with individual differences in stress reactivity. In upcoming work, we will manipulate levels of gene expression of these candidate genes in behaving rats to address causal links to anxiety.
  2. Loneliness: Why don’t lonely individuals experience “social lifts”? Is loneliness associated with differential gene expression in the neural circuitry of reward?  Loneliness is a subjective state of mind, independent of one’s social network size, and therefore difficult to study in non-human animals. A better understanding of the biology of loneliness is motivated by the fact that it is associated with profound adverse mental (affective/social, cognitive) and physical health consequences. We are currently studying the gene expression profile in postmortem tissue from MAP donors with known levels of loneliness to investigate links between loneliness and health.
  3. Purpose in Life: How does “Purpose in Life” promote healthy aging, and protect against Alzheimer’s disease? My collaborators Patricia Boyle and David Bennett made a surprising discovery in longitudinal studies of aging in community-based populations: that “Purpose in Life”, which is the “psychological tendency to derive meaning from life’s experiences and possess a sense of intentionality and goal directedness”, is associated with significantly reduced mortality and even with reduced risk of Alzheimer’s disease, even after controlling for a large number of confounds. Based on the hypothesis that Purpose acts as a psychosocial buffer, we recently showed that scores in Purpose in Lifepredicted physiological responses to social stress: using the Trier Social Stress Test, we found that cortisol stress hormone levels returned to pre-stress baseline levels faster in participants who had a high level of Purpose [10].
  4. Hunting for Depression Pathogens . In upcoming work, we will use a gene expression chip designed in my lab to begin the search for pathogens associated with depression. Our chip contains more than 100,000 probes for a variety of pathogens.

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