Dr. M. Maes organizes a symposium at the World Psychiatric Association Congress,
Florence, Italy, April 2009: Common inflammatory pathways underpinning depression, chronic fatigue and somatization : novel pathways and new drug-targets.
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Bron: Michael Maes
Datum: Juni 2008
URL: http://www.ediver.be...t news/news.htm
Ref: http://www.wpa2009florence.org/
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Symposia,
http://www.wpa2009fl...tesymposia.html
http://www.wpa2009fl...rg/regular.html
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Chairs: M. Abouh-Sale and M. Maes
Speakers: 1. S. Riemer, University of Marburg, Department of Clinical
Psychology and Psychotherapy, Germany.
2. B. Leonard, Department of Psychiatry and Psychotherapy, Ludwig
Maximilian University, Munich, Germany.
3. K. De Meirleir, University of Brussels, Brussels, Belgium; 4. M. Maes, Clinical Research Center for Mental Health, Antwerp,
Belgium.
The aim of this symposium is to review the current knowledge on the common
pathways underpinning major depression (MDD) and somatiform disorder and
chronic fatigue syndrome (CFS). Those novel pathways are amongst others:
inflammatory reactions, including intracellular inflammation; lowered
tryptophan levels with increased TRYCAT (tryptophan catabolites along the
IDO pathway) concentrations; lowered omega-3 fatty acid levels; increased
oxidative & nitrosative stress (O&NS) and damage to functional proteins and
lipid membrane structures by O&NS; and an increased gut permeability.
S. Riemer will review the first research data obtained in patients with
somatiform disorder as compared to depressed patients and normal controls:
increased signs of inflammation, lowered tryptophan levels and lowered
omega-3 polyunsaturated fatty acids are shown to occur in depression and
somatiform disorder as well.
B. Leonard will present data that depression may be an immunological disorder
characterized by increased levels of inflammatory cytokines and an increased
activity of cyclo-oxygenase 2 and nitric oxide synthase in the brain, which
eventually may cause neuronal apoptosis in the hippocampus and neocortex.
Pro-inflammatory cytokines also stimulate the kynurenine pathway leading to
the synthesis of the neurotoxin quinolinic acid.
K. De Meirleir will review his data that CFS is accompanied by several immune
disorders, such as disorders in PKR, RNase-L, elastase, natural killer cell
activity, etc. He will show that O&NS through an increased production of iNOS
and NO may induce "psychosomatic symptoms", such as those occurring in
CFS, e.g. fatigue, pain and autonomic symptoms.
M. Maes will review his data that the comorbidity between MDD and CFS may be
explained by a number of inflammatory pathways, e.g. increased intracellular
inflammation, lower omega-3 PUFA levels, increased O&NS and damage to
functional proteins and membrane lipid structures caused by O&NS, and
intestinal mucosal dysfunction. It is concluded that a) "functional" or
"psychosomatic" symptoms have a genuine organic pathophysiology, i.e.
disturbances in inflammatory pathways; and
the development of new drugs,aimed at treating depression, CFS, and somatiform disorder, should target
those novel inflammatory, O&NS and IMD pathways.
