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Neuropsychiatric Disorders

Senior Researchers:

Professor Elias Eriksson

Professor Ingmar Skoog

Professor Deborah Gustafson

To further explore the hypothesis that a major physiological role of the brain neurotransmitter serotonin is to modulate SS-driven behavior, researchers in this module will analyze how SS influence gene expression in various parts of the brain (e.g., amygdala), using microarrays and determine the extent to which these effects are modulated or mediated by serotonergic neurons. Genetically modified mice that over- or underexpress genes relevant to serotonin transmission or genes of importance for SS activity will be used.

Connexins are gap junction proteins that appear to be critical for synchronizing electrical activity of neurons and for brain development. Estrogens regulate the expression of connexins in several tissues, including the brain. CEROSS-affiliated researcher Lars Westberg, currently in the lab of Donald Pfaff (Rockefeller University, New York), is studying the relevance of gap junctions for the behavioral effects of estrogen in the hypothalamus. When Dr. Westberg returns to Göteborg in 2006, this work will be pursued within the framework of CEROSS, partly in collaboration with Dr. Pfaff.

The clinical studies of Dr Eriksson and co-workers on the effect of serotonin reuptake inhibitors (SRIs) in premenstrual dysphoric disorder will be pursued. Their recent finding that an androgen antagonist may reduce the symptoms of bulimia nervosa will be explored in a new trial. The possible efficacy of androgen antagonist for other serotonin-related conditions in women will be explored.

Women with premenstrual dysphoric disorder will be compared to women with no such complaints with respect to a large number of polymorphisms in SS-related genes, in collaboration with professor Meir Steiner (McMaster University, Ontario, Canada) and professor David Rubinow (NIMH, Bethesda, USA).

The possible involvement of SS-related genes in large well-defined populations of subjects with autism and attention deficit hyperactivity disorder, and in first-degree relatives, will be studied in collaboration with professor Marion Leboyer (INSERM, Paris) and Professor Christopher Gillberg (Göteborg).The possible role of SS-related genes in other psychiatric disorders displaying marked sex differences in prevalence, such as depression, anxiety disorders, and eating disorders, will also be explored.

There are subtle but reproducible sex differences in various aspects of cognitive function. Through a collaboration with Professor Lars-Göran Nilsson (Stockholm University), Eriksson and co-workers have access to DNA from a large population-recruited cohort of men and women (BETULA, n = 3000) who have been studied extensively with respect to cognitive function and followed longitudinally for decades. In these subjects, the relationship between SS-related genes and cognitive performance will be assessed.

In collaboration with professor Paul Lichtenstein (Swedish Twin Registry), they will address the putative influence of prenatal androgen exposure on a variety of mental and somatic traits, by comparing female heterozygotic twins who have twin brothers to female heterozygotic twins who have twin sisters. The Swedish Twin Registry has the largest twin populations in the world.

The role of SS in psychiatric disorders will be addressed in well-characterized longitudinal epidemiological studies, led by Dr Skoog. Partly unique cohorts that have been studied longitudinally and in detail for several decades will be investigated, including the H70 Study, the 95 Study, the Prospective Population Study on Women (PPSW), and the Birth Cohort Study of 70-year-olds in Göteborg.

The following assessments and examinations are being undertaken in these cohorts: 1) Structured assessments of psychiatric symptoms and signs, including personality inventories and questions on suicidal feelings, sexuality, and sleep, as well as cognitive tests. 2) Close informant interviews. 3) Assessment of physical status, history of medical conditions (including cardiovascular disorders, diabetes mellitus, hip fracture and cancer), psychosocial factors, anthropometric measurements, blood pressure, and ECG. 4) Collection of blood (serum, plasma, and whole blood for DNA analysis), DNA so far having been extracted on 1500 participants. 5)

Brain imaging in the form of CT providing measures of brain atrophy, ventricular enlargement, white matter lesions, infarcts and basal ganglia, calcifications, 1500 CT examinations having been undertaken so far. 6) Cerebrospinal fluid (CSF) analyses, including assessment of e.g. Ab-42, T-tau, apoE, and CSF/blood albumin ratio.

These data will be analyzed to explore the influence of SS on the risk of developing AD, cognitive decline, age-related brain changes, and other psychiatric disorders (such as depression) and on adiposity measures. Serum levels of SS and sex-hormone-binding globulin will be measured in previously collected and stored blood samples, as well as in future samples. Extensive analysis of polymorphisms and mutations in SS-related genes will also be undertaken. The role of exogenous hormones (hormone replacement therapy) also will be assessed.

In a recent publication, Dr Skoog and co-workers showed that obesity is a risk factor for AD in women. For the studies on the role of SS for the metabolic syndrome conducted within module 5, the cohorts described above will be used, with special focus on the possible role of SS.

Page Manager: Marie Lagerquist|Last update: 12/10/2010
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