P.0512 Brain serotonin transporter is associated with cognitive affective biases in healthy individuals

2021 ◽  
Vol 53 ◽  
pp. S377-S378
Author(s):  
S. Armand ◽  
B. Ozenne ◽  
N. Svart ◽  
V.G. Frøkjær ◽  
G.M. Knudsen ◽  
...  
2014 ◽  
Vol 10 ◽  
pp. 1744-8069-10-76 ◽  
Author(s):  
Ellen Lund Schaldemose ◽  
Emilia Horjales-Araujo ◽  
Ditte Demontis ◽  
Anders D Eørglum ◽  
Peter Svensson ◽  
...  

1993 ◽  
Vol 60 (6) ◽  
pp. 2319-2322 ◽  
Author(s):  
Klaus-Peter Lesch ◽  
Benjamin L. Wolozin ◽  
Dennis L. Murphy ◽  
Peter Riederer

2019 ◽  
Vol 54 (3) ◽  
pp. 209-215 ◽  
Author(s):  
Christine Muench ◽  
Audrey Luo ◽  
Katrin Charlet ◽  
Jisoo Lee ◽  
Daniel B Rosoff ◽  
...  

Abstract Aims Differences in DNA methylation of the serotonin transporter gene (SLC6A4) have been shown to alter SLC6A4 expression and predict brain functions in healthy individuals. This study investigated the association between SLC6A4 promoter methylation and threat-related amygdala activation in individuals with alcohol dependence (AD). Methods Methylation of the SLC6A4 promoter region was assessed using peripheral blood DNA from 45 individuals with AD and 45 healthy controls (HCs). All participants completed an emotional face matching task in a 3-T magnetic resonance imaging (MRI) scanner. Results Results did not reveal any association between SLC6A4 promoter methylation variation and threat-related amygdala activation in HCs or individuals with AD. Furthermore, methylation in the promoter region of SLC6A4 did not significantly differ between the groups. Conclusions Our results do not replicate a previous finding that increased methylation in the promoter region of SLC6A4 is associated with threat-related amygdala activation in healthy individuals and further show that there is no such association in individuals with AD. Given that the number of imaging epigenetics studies on SLC6A4 is very limited to date, these inconsistent results indicate that future research is needed to clarify its association with amygdala reactivity in both healthy and clinical populations.


1995 ◽  
Vol 23 (1) ◽  
pp. 40S-40S
Author(s):  
HELOISE M. TARRANT ◽  
D. CLIVE WILLIAMS

NeuroImage ◽  
2006 ◽  
Vol 31 ◽  
pp. T41
Author(s):  
J. John Mann ◽  
M. Oquendo ◽  
V. Arango ◽  
T. Ogdon ◽  
R. van Heertum ◽  
...  

2009 ◽  
Vol 194 (4) ◽  
pp. 355-359 ◽  
Author(s):  
Sudhakar Selvaraj ◽  
Rosa Hoshi ◽  
Zubin Bhagwagar ◽  
Naga Venkatesha Murthy ◽  
Rainer Hinz ◽  
...  

BackgroundAnimal experimental studies have prompted concerns that widespread use of 3,4-methylenedioxymethamphetamine (MDMA; ‘ecstasy’) by young people may pose a major public health problem in terms of persistent serotonin neurotoxicity.AimsTo determine the status of brain serotonin neurons in a group of abstinent MDMA users.MethodWe assessed the integrity of brain serotonin neurons by measuring serotonin transporter (SERT) binding using positron emission tomography (PET) and [11C]DASB in 12 former MDMA users, 9 polydrug users who had never taken MDMA and 19 controls who reported no history of illicit drug use.ResultsThere was no significant difference in the binding potential of [11C]DASB between the groups in any of the brain regions examined.ConclusionsTo the extent that [11C]DASB binding provides an index of the integrity of serotonin neurons, our findings suggest that MDMA use may not result in long-term damage to serotonin neurons when used recreationally in humans.


NeuroImage ◽  
2009 ◽  
Vol 47 ◽  
pp. S89
Author(s):  
Y Ouchi ◽  
E Yoshikawa ◽  
M Futatsubashi ◽  
T Kanno ◽  
S Yagi ◽  
...  

2000 ◽  
Vol 47 (6) ◽  
pp. 482-489 ◽  
Author(s):  
Matthäus Willeit ◽  
Nicole Praschak-Rieder ◽  
Alexander Neumeister ◽  
Walter Pirker ◽  
Susanne Asenbaum ◽  
...  

2008 ◽  
Vol 65 (9) ◽  
pp. 1072 ◽  
Author(s):  
Nicole Praschak-Rieder ◽  
Matthaeus Willeit ◽  
Alan A. Wilson ◽  
Sylvain Houle ◽  
Jeffrey H. Meyer

2008 ◽  
Vol 18 (4) ◽  
pp. 167-176 ◽  
Author(s):  
Anastasiya V. Kazantseva ◽  
Daria A. Gaysina ◽  
Gulnaz G. Faskhutdinova ◽  
Tatyana Noskova ◽  
Sergey B. Malykh ◽  
...  

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