SwePub
Sök i SwePub databas

  Utökad sökning

AND är defaultoperator och kan utelämnas

Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Basic Medicine) ;pers:(Eriksson Elias 1956)"

Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES Basic Medicine) > Eriksson Elias 1956

  • Resultat 1-10 av 135
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Näslund, Jakob, et al. (författare)
  • Expression of 22 serotonin-related genes in rat brain after sub-acute serotonin depletion or reuptake inhibition
  • 2020
  • Ingår i: Acta Neuropsychiatrica. - : Cambridge University Press (CUP). - 0924-2708 .- 1601-5215. ; 32:3, s. 159-165
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Although the assessment of expression of serotonin-related genes in experimental animals has become a common strategy to shed light on variations in brain serotonergic function, it remains largely unknown to what extent the manipulation of serotonin levels causes detectable changes in gene expression. We therefore chose to investigate how sub-acute depletion or elevation of brain serotonin influences the expression of a number of serotonin-related genes in six brain areas. Methods: Male Wistar rats were administered a serotonin synthesis inhibitor, para-chlorophenylalanine (p-CPA), or a serotonin reuptake inhibitor, paroxetine, for 3 days and then sacrificed. The expression of a number of serotonin-related genes in the raphe nuclei, hypothalamus, amygdala, striatum, hippocampus and prefrontal cortex was investigated using real-time quantitative PCR (rt-qPCR). Results: While most of the studied genes were uninfluenced by paroxetine treatment, we could observe a robust downregulation of tryptophan hydroxylase-2 in the brain region where the serotonergic cell bodies reside, that is, the raphe nuclei. p-CPA induced a significant increase in the expression of Htr1b and Htr2a in amygdala and of Htr2c in the striatum and a marked reduction in the expression of Htr6 in prefrontal cortex; it also enhanced the expression of the brain-derived neurotrophic factor (Bdnf) in raphe and hippocampus. Conclusion: With some notable exceptions, the expression of most of the studied genes is left unchanged by short-term modulation of extracellular levels of serotonin.
  •  
2.
  • Frick, Andreas, Docent, et al. (författare)
  • Neuroimaging, genetic, clinical, and demographic predictors of treatment response in patients with social anxiety disorder
  • 2020
  • Ingår i: Journal of Affective Disorders. - : Elsevier BV. - 0165-0327 .- 1573-2517. ; 261, s. 230-237
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Correct prediction of treatment response is a central goal of precision psychiatry. Here, we tested the predictive accuracy of a variety of pre-treatment patient characteristics, including clinical, demographic, molecular genetic, and neuroimaging markers, for treatment response in patients with social anxiety disorder (SAD). Methods: Forty-seven SAD patients (mean±SD age 33.9 ± 9.4 years, 24 women) were randomized and commenced 9 weeks’ Internet-delivered cognitive behavior therapy (CBT) combined either with the selective serotonin reuptake inhibitor (SSRI) escitalopram (20 mg daily [10 mg first week], SSRI+CBT, n = 24) or placebo (placebo+CBT, n = 23). Treatment responders were defined from the Clinical Global Impression-Improvement scale (CGI-I ≤ 2). Before treatment, patients underwent functional magnetic resonance imaging and the Multi-Source Interference Task taxing cognitive interference. Support vector machines (SVMs) were trained to separate responders from nonresponders based on pre-treatment neural reactivity in the dorsal anterior cingulate cortex (dACC), amygdala, and occipital cortex, as well as molecular genetic, demographic, and clinical data. SVM models were tested using leave-one-subject-out cross-validation. Results: The best model separated treatment responders (n = 24) from nonresponders based on pre-treatment dACC reactivity (83% accuracy, P = 0.001). Responders had greater pre-treatment dACC reactivity than nonresponders especially in the SSRI+CBT group. No other variable was associated with clinical response or added predictive accuracy to the dACC SVM model. Limitations: Small sample size, especially for genetic analyses. No replication or validation samples were available. Conclusions: The findings demonstrate that treatment outcome predictions based on neural cingulate activity, at the individual level, outperform genetic, demographic, and clinical variables for medication-assisted Internet-delivered CBT, supporting the use of neuroimaging in precision psychiatry.
  •  
3.
  • Lisinski, Alexander, 1989, et al. (författare)
  • Item-based analysis of the effects of duloxetine in depression: a patient-level post hoc study
  • 2020
  • Ingår i: Neuropsychopharmacology. - : Springer Science and Business Media LLC. - 1740-634X .- 0893-133X. ; 45:3, s. 553-560
  • Tidskriftsartikel (refereegranskat)abstract
    • Oft-cited trial-level meta-analyses casting doubt on the usefulness of antidepressants have been based on re-analyses of to what extent the active drug has outperformed placebo in reducing the sum score of the Hamilton Depression Rating Scale (HDRS-17-sum) in clinical trials. Recent studies, however, suggest patient-level analyses of individual HDRS items to be more informative when assessing the efficacy of an antidepressant. To shed further light on both symptom-reducing and symptom-aggravating effects of a serotonin and noradrenaline reuptake inhibitor, duloxetine, when used for major depression in adults, we hence applied this approach to re-analyse data from 13 placebo-controlled trials. In addition, using patient-level data from 28 placebo-controlled trials of selective serotonin reuptake inhibitors (SSRIs), the response profile of duloxetine was compared to that of these drugs. Duloxetine induced a robust reduction in depressed mood that was not dependent on baseline severity and not caused by side-effects breaking the blind. A beneficial effect on depressed mood was at hand already after one week; when outcome was assessed using HDRS-17-sum as effect parameter, this early response was however masked by a concomitant deterioration with respect to adverse event-related items. No support for a suicide-provoking effect of duloxetine was obtained. The response profile of duloxetine was strikingly similar to that of the SSRIs. We conclude that the use of HDRS-17-sum as effect parameter underestimates the true efficacy and masks an early effect of duloxetine on core symptoms of depression. No support for major differences between duloxetine and SSRIs in clinical profile were obtained.
  •  
4.
  • Furmark, Tomas, et al. (författare)
  • A link between serotonin-related gene polymorphisms, amygdala activity, and placebo-induced relief from social anxiety
  • 2008
  • Ingår i: Journal of Neuroscience. - 0270-6474 .- 1529-2401. ; 28:49, s. 13066-74
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
  •  
5.
  • Furmark, Tomas, et al. (författare)
  • Genotype over-diagnosis in amygdala responsiveness: affective processing in social anxiety disorder.
  • 2009
  • Ingår i: Journal of psychiatry & neuroscience : JPN. - : Canadian Medical Association. - 1488-2434 .- 1180-4882. ; 34:1, s. 30-40
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Although the amygdala is thought to be a crucial brain region for negative affect, neuroimaging studies do not always show enhanced amygdala response to aversive stimuli in patients with anxiety disorders. Serotonin (5-HT)-related genotypes may contribute to interindividual variability in amygdala responsiveness. The short (s) allele of the 5-HT transporter linked polymorphic region (5-HTTLPR) and the T variant of the G-703T polymorphism in the tryptophan hydroxylase-2 (TPH2) gene have previously been associated with amygdala hyperresponsivity to negative faces in healthy controls. We investigated the influence of these polymorphisms on amygdala responsiveness to angry faces in patients with social anxiety disorder (SAD) compared with healthy controls. METHODS: We used positron emission tomography with oxygen 15-labelled water to assess regional cerebral blood flow in 34 patients with SAD and 18 controls who viewed photographs of angry and neutral faces presented in counterbalanced order. We genotyped all participants with respect to the 5-HTTLPR and TPH2 polymorphisms. RESULTS: Patients with SAD and controls had increased left amygdala activation in response to angry compared with neutral faces. Genotype but not diagnosis explained a significant portion of the variance in amygdala responsiveness, the response being more pronounced in carriers of s and/or T alleles. LIMITATIONS: Our analyses were limited owing to the small sample and the fact that we were unable to match participants on genotype before enrollment. In addition, other imaging techniques not used in our study may have revealed additional effects of emotional stimuli. CONCLUSION: Amygdala responsiveness to angry faces was more strongly related to serotonergic polymorphisms than to diagnosis of SAD. Emotion activation studies comparing amygdala excitability in patient and control groups could benefit from taking variation in 5-HT-related genes into account.
  •  
6.
  • Lisinski, Alexander, 1989, et al. (författare)
  • Impact of chosen cutoff on response rate differences between selective serotonin reuptake inhibitors and placebo
  • 2022
  • Ingår i: Translational Psychiatry. - : Springer Science and Business Media LLC. - 2158-3188. ; 12:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Response defined as a 50% reduction in the sum score of the Hamilton Depression Rating Scale (HDRS-17-sum) is often used to assess the efficacy of antidepressants. Critics have, however, argued that dichotomising ratings with a cutoff close to the median may lead to scores clustering on either side, the result being inflation of miniscule drug-placebo differences. Using pooled patient-level data sets from trials of three selective serotonin reuptake inhibitors (SSRIs) (citalopram, paroxetine and sertraline) (n = 7909), and from similar trials of duloxetine (n = 3478), we thus assessed the impact of different cutoffs on response rates. Response criteria were based on (i) HDRS-17-sum, (ii) the sum score of the HDRS-6 subscale (HDRS-6-sum) and (iii) the depressed mood item. The separation between SSRI and placebo with respect to response rates increased when HDRS-17-sum was replaced by HDRS-6-sum or depressed mood as effect parameter and was markedly dependent on SSRI dose. With the exception of extreme cutoff values, differences in response rates were largely similar regardless of where the cutoff was placed, and also not markedly changed by the exclusion of subjects close to the selected cutoff (e.g., +/- 10%). The observation of similar response rate differences between active drugs and placebo for different cutoffs was corroborated by the analysis of duloxetine data. In conclusion, the suggestion that using a cutoff close to the median when defining response has markedly overestimated the separation between antidepressants and placebo may be discarded.
  •  
7.
  • Kauppi, Karolina, et al. (författare)
  • KIBRA polymorphism is related to enhanced memory and elevated hippocampal processing.
  • 2011
  • Ingår i: The Journal of neuroscience : the official journal of the Society for Neuroscience. - : Society for Neuroscience. - 1529-2401 .- 0270-6474. ; 31:40, s. 14218-22
  • Tidskriftsartikel (refereegranskat)abstract
    • Several studies have linked the KIBRA rs17070145 T polymorphism to superior episodic memory in healthy humans. One study investigated the effect of KIBRA on brain activation patterns (Papassotiropoulos et al., 2006) and observed increased hippocampal activation in noncarriers of the T allele during retrieval. Noncarriers were interpreted to need more hippocampal activation to reach the same performance level as T carriers. Using large behavioral (N = 2230) and fMRI (N = 83) samples, we replicated the KIBRA effect on episodic memory performance, but found increased hippocampal activation in T carriers during episodic retrieval. There was no evidence of compensatory brain activation in noncarriers within the hippocampal region. In the main fMRI sample, T carriers performed better than noncarriers during scanning but, importantly, the difference in hippocampus activation remained after post hoc matching according to performance, sex, and age (N = 64). These findings link enhanced memory performance in KIBRA T allele carriers to elevated hippocampal functioning, rather than to neural compensation in noncarriers.
  •  
8.
  • de Frias, Cindy M, et al. (författare)
  • COMT gene polymorphism is associated with declarative memory in adulthood and old age.
  • 2004
  • Ingår i: Behavior genetics. - New York : Kluwer Academic Publishers. - 0001-8244 .- 1573-3297. ; 34:5, s. 533-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Variation in memory performance is to a large extent explained by genes. In the prefrontal cortex, the catechol O-methyltransferase (COMT) gene is essential in the metabolic degradation of dopamine, a neurotransmitter implicated in cognitive functions. The present study examined the effect of a polymorphism in the COMT gene on individual differences and changes in memory in adulthood and old age. Tests assessing episodic and semantic memory were administered to 286 men (initially aged 35-85 years) from a random sample of the population (i.e., the Betula prospective cohort study) at two occasions followed over a 5-year period. Carriers of the Met/Met genotype (with low enzyme activity) performed better on episodic and semantic memory, as compared to carriers of the Val allele (with higher enzyme activity). Division of episodic memory into its recall and recognition components showed that the difference was specific to episodic recall, not recognition tasks; an effect that was observed across three age groups (middle-age, young-old, and old-old adults) and over a 5-year period. The COMT gene is a plausible candidate gene for memory functioning in adulthood and old age.
  •  
9.
  • Andersson, Evelyn, et al. (författare)
  • Genetic Polymorphisms in Monoamine Systems and Outcome of Cognitive Behavior Therapy for Social Anxiety Disorder
  • 2013
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:11
  • Tidskriftsartikel (refereegranskat)abstract
    • ObjectiveThe role of genetics for predicting the response to cognitive behavior therapy (CBT) for social anxiety disorder (SAD) has only been studied in one previous investigation. The serotonin transporter (5-HTTLPR), the catechol-o-methyltransferase (COMT) val158met, and the tryptophan hydroxylase-2 (TPH2) G-703Tpolymorphisms are implicated in the regulation of amygdala reactivity and fear extinction and therefore might be of relevance for CBT outcome. The aim of the present study was to investigate if these three gene variants predicted response to CBT in a large sample of SAD patients.MethodParticipants were recruited from two separate randomized controlled CBT trials (trial 1: n = 112, trial 2: n = 202). Genotyping were performed on DNA extracted from blood or saliva samples. Effects were analyzed at follow-up (6 or 12 months after treatment) for both groups and for each group separately at post-treatment. The main outcome measure was the Liebowitz Social Anxiety Scale Self-Report.ResultsAt long-term follow-up, there was no effect of any genotype, or gene × gene interactions, on treatment response. In the subsamples, there was time by genotype interaction effects indicating an influence of the TPH2 G-703T-polymorphism on CBT short-term response, however the direction of the effect was not consistent across trials.ConclusionsNone of the three gene variants, 5-HTTLPR, COMTval158met and TPH2 G-703T, was associated with long-term response to CBT for SAD.
  •  
10.
  • Hedner, Margareta, et al. (författare)
  • Age-Related Olfactory Decline is Associated with the BDNF Val66met Polymorphism : Evidence from a Population-Based Study
  • 2010
  • Ingår i: Frontiers in Aging Neuroscience. - : Frontiers Media SA. - 1663-4365. ; 2:7, s. 24-
  • Tidskriftsartikel (refereegranskat)abstract
    • The present study investigates the effect of the brain-derived neurotrophic factor (BDNF) val66met polymorphism on change in olfactory function in a large scale, longitudinal population-based sample (n = 836). The subjects were tested on a 13 item force-choice odor identification test on two test occasions over a 5-year-interval. Sex, education, health-related factors, and semantic ability were controlled for in the statistical analyses. Results showed an interaction effect of age and BDNF val66met on olfactory change, such that the magnitude of olfactory decline in the older age cohort (70–90years old at baseline) was larger for the val homozygote carriers than for the met carriers. The older met carriers did not display larger age-related decline in olfactory function compared to the younger group. The BDNF val66met polymorphism did not affect the rate of decline in the younger age cohort (45–65years). The findings are discussed in the light of the proposed roles of BDNF in neural development and maintenance.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 135
Typ av publikation
tidskriftsartikel (128)
konferensbidrag (3)
bokkapitel (3)
forskningsöversikt (1)
Typ av innehåll
refereegranskat (127)
övrigt vetenskapligt/konstnärligt (8)
Författare/redaktör
Westberg, Lars, 1973 (38)
Landén, Mikael, 1966 (20)
Holm, Göran, 1942 (18)
Nilsson, Staffan, 19 ... (17)
Annerbrink, Kristina ... (17)
visa fler...
Henningsson, Susanne ... (16)
Rosmond, Roland, 196 ... (16)
Olsson, Marie, 1971 (15)
Hieronymus, Fredrik (14)
Baghaei, Fariba, 196 ... (13)
Nilsson, Lars-Göran (11)
Björntorp, Per, 1931 (11)
Lisinski, Alexander, ... (11)
Ekman, Agneta, 1961 (10)
Hellstrand, Monika, ... (10)
Melke, Jonas, 1971 (10)
Ho, Hoi-Por, 1962 (9)
Nissbrandt, Hans, 19 ... (8)
Holmäng, Agneta, 195 ... (8)
Allgulander, Christe ... (8)
Adolfsson, Rolf (7)
Bergman, Olle, 1978 (7)
Fredrikson, Mats (6)
Furmark, Tomas (6)
Bah Rösman, Jessica, ... (6)
Sundblad-Elverfors, ... (6)
Studer, Erik (6)
Nilsson, Cecilia (5)
Hedner, Jan A, 1953 (5)
Andersch, Sven, 1939 (5)
Zetterberg, Henrik, ... (4)
Jennische, Eva, 1949 (4)
Nyberg, Lars (4)
Bäckström, Torbjörn (4)
Håkansson, Anna, 197 ... (4)
Sjödin, Ingemar (4)
Epperson, C. Neill (4)
Dennerstein, Lorrain ... (4)
Appel, Lieuwe (3)
Faria, Vanda (3)
Suchankova, Petra, 1 ... (3)
Melchior, Lydia K, 1 ... (3)
Schmidt, Peter (3)
Åhs, Fredrik (3)
Santtila, Pekka (3)
Herlitz, Agneta (3)
Andersch, Björn (3)
de Frias, Cindy M. (3)
Emilsson, Johan Fred ... (3)
visa färre...
Lärosäte
Göteborgs universitet (126)
Karolinska Institutet (19)
Chalmers tekniska högskola (17)
Umeå universitet (14)
Uppsala universitet (11)
Stockholms universitet (5)
visa fler...
Linköpings universitet (5)
Lunds universitet (5)
Mittuniversitetet (2)
Mälardalens universitet (1)
Örebro universitet (1)
visa färre...
Språk
Engelska (132)
Svenska (3)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (135)
Samhällsvetenskap (16)
Naturvetenskap (2)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy