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Author Topic: Wo die Placebowirkung im Gehirn entsteht  (Read 1240 times)

ama

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Wo die Placebowirkung im Gehirn entsteht
« on: December 06, 2008, 05:36:17 PM »

Zitat aus http://www.aerzteblatt.de/v4/news/news.asp?id=34666

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Das Placebo-Gen – Warum nicht jeder auf Scheinmedikamente anspricht

Donnerstag, 4. Dezember 2008

Uppsala – Schwedische Forscher haben entdeckt, wo die Placebowirkung im
Gehirn entsteht. Ihre Studie im Journal of Neuroscience (2008; 28:
13066-13074) zeigt außerdem, dass die Wirkung an ein bestimmtes Gen
gebunden ist.

Links zum Thema
» Abstract der Studie
http://www.jneurosci.org/cgi/content/abstract/28/49/13066

» Pressemitteilung der Universität Uppsala
http://www.eurekalert.org/pub_releases/2008-12/uu-gdw120308.php
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Der Abstract:

http://www.jneurosci.org/cgi/content/abstract/28/49/13066

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The Journal of Neuroscience,December 3, 2008,
28(49):13066-13074; doi:10.1523/JNEUROSCI.2534-08.2008

Behavioral/Systems/Cognitive

A Link between Serotonin-Related Gene Polymorphisms, Amygdala Activity,
and Placebo-Induced Relief from Social Anxiety


Tomas Furmark,1 Lieuwe Appel,2 Susanne Henningsson,3 Fredrik Åhs,1 Vanda Faria,1
Clas Linnman,1 Anna Pissiota,1 Örjan Frans,1 Massimo Bani,4 Paolo Bettica,4
Emilio Merlo Pich,4 Eva Jacobsson,5 Kurt Wahlstedt,5 Lars Oreland,6 Bengt Långström,2,7
Elias Eriksson,3 and Mats Fredrikson1

1Department of Psychology, Uppsala University, SE-751 42 Uppsala, Sweden,
2Uppsala Imanet, GE Healthcare, SE-751 09 Uppsala, Sweden,
3Department of Pharmacology, Göteborg University, SE-405 30 Göteborg,
Sweden,
4GlaxoSmithKline, Medicine Research Centre, 37135 Verona, Italy,
5Quintiles AB Phase I Services, SE-753 23 Uppsala, Sweden,
6Department of Neuroscience, Pharmacology, Uppsala University, SE-751 24
Uppsala, Sweden, and
7Department of Biochemistry and Organic Chemistry, Uppsala University,
SE-751 23 Uppsala, Sweden

Correspondence should be addressed to Dr. Tomas Furmark, Department of
Psychology, Uppsala University, Box 1225, SE-751 42 Uppsala, Sweden.
Email: <tomas.furmark[bat]psyk.uu.se>

Placebo may yield beneficial effects that are indistinguishable from those
of active medication, but the factors underlying proneness to respond to
placebo are widely unknown. Here, we used functional neuroimaging to
examine neural correlates of anxiety reduction resulting from sustained
placebo treatment under randomized double-blind conditions, in patients
with social anxiety disorder. Brain activity was assessed during a
stressful public speaking task by means of positron emission tomography
before and after an 8 week treatment period. Patients were genotyped with
respect to the serotonin transporter-linked polymorphic region (5-HTTLPR)
and the G-703T polymorphism in the tryptophan hydroxylase-2 (TPH2) gene
promoter. Results showed that placebo response was accompanied by reduced
stress-related activity in the amygdala, a brain region crucial for
emotional processing. However, attenuated amygdala activity was
demonstrable only in subjects who were homozygous for the long allele of
the 5-HTTLPR or the G variant of the TPH2 G-703T polymorphism, and not in
carriers of short or T alleles. Moreover, the TPH2 polymorphism was a
significant predictor of clinical placebo response, homozygosity for the G
allele being associated with greater improvement in anxiety symptoms. Path
analysis supported that the genetic effect on symptomatic improvement with
placebo is mediated by its effect on amygdala activity. Hence, our study
shows, for the first time, evidence of a link between genetically
controlled serotonergic modulation of amygdala activity and
placebo-induced anxiety relief.

Key words:
placebo; genes; phobia; serotonin; brain; functional neuroimaging

Received June 4, 2008; revised Sept. 29, 2008; accepted Oct. 22, 2008.

Correspondence should be addressed to
Dr. Tomas Furmark
Department of Psychology
Uppsala University
Box 1225, SE-751 42
Uppsala
Sweden
Email: <tomas.furmark[bat]psyk.uu.se>
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The press release:

http://www.eurekalert.org/pub_releases/2008-12/uu-gdw120308.php

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Public release date: 3-Dec-2008

Contact: Tomas Furmark
tomas.furmark[bat]psyk.uu.se
46-073-683-3487
Uppsala University

Genes determine whether sugar pills work

It is a well-known fact in drug trials that individuals can respond just
as well to placebos, sugar pills, as to the active drug. On the other
hand, it is difficult to explain why only certain people get better from
placebos. A team of researchers from Uppsala University and Gothenburg
University have now found gene variants that can impact the placebo effect
and a mechanism in the brain that characterizes those who respond to
placebos.
The study, published in Journal of Neuroscience, examined 108 individuals
suffering from social phobia using a brain camera (PET, positron emission
tomography). The individuals were participating in a treatment study
looking into how anxiety-moderating drugs affect brain activity. Just
under one fourth of the subjects were given a placebo instead of a drug.
This was a double-blind study, meaning that neither the subjects nor the
research team know who was taking the drug or the sugar pill.

Before and after an eight-week period of treatment, the participants were
asked to give a stressful oral presentation while their brain activity was
monitored. When all the metering was finished and the study was decoded,
it turned out that 40 percent of the placebo group had received the same
degree of anxiety relief from the sugar pill as other groups got from a
drug.
Those who responded well to the placebo had a significant reduction in
activity in the amygdala in the temporal lobe, while this reduction was
not found in the others. In previous research the amygdala has stood out
as a key structure for emotional reactions. Both serotonin-active drugs
(SSRI preparations) and cognitive behavioral therapy moderate activity in
this area.
"Thus, successful placebo treatment works through the same mechanism in
the brain," says Tomas Furmark at the Uppsala University Department of
Psychology, who directed the study.

The study also analyzed two genes that influence the reabsorption and
synthesis of serotonin in the brain (the serotonin transporter gene and
the tryptophan hydroxylase-2 gene). The findings showed that only
individuals who had certain variants, alleles, of these genes had a
moderation of activity in the amygdala. Above all, the tryptophan
hydroxylase-2 genes variants could predict the degree of relief from
anxiety achieved by the placebo pill as well as the moderation of the
amygdala.

Statistical analyses showed that it is a genetic effect on the activity in
the amygdala that influences the propensity to respond to a placebo, that
is, a path from the gene, via the brain, to behavior.

The study shows for the first time that genes influence the placebo effect
by regulating the propensity to react in an area of the brain that is
important for our feelings.

This could have significant consequences for all drug testing and other
treatment studies that use a placebo.

"The findings show that the possibilities of demonstrating that an active
treatment functions better than a placebo can be affected by the gene
variants in the trial subjects. It is also possible that genes can explain
why certain people respond well or poorly to anxiety-moderating drugs and
psychotherapy respectively," says Tomas Furmark.
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Kommentar aus dem Hintergrund:

"Emotion ist keine Emotion, sondern eine Computersteuerung durch die älteren Hirnteile.

Das dürfte auch ziemlich hoch damit korrelieren, daß Esoteriker NICHT denken WOLLEN."



Ich glaube, jetzt haben die Esoteriker ein ernstes Problem: Sie sind im Vollbesitz eines Gendefekts...

.
« Last Edit: December 06, 2008, 05:37:22 PM by ama »
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