623 research outputs found
282 INCREASED SENSITIVITY TO PAIN FOLLOWING A SINGLE OPIATE DOSE IS INFLUENCED BY THE COMT val158met POLYMORPHISM
No full textJensen K, Lonsdorf T, Schalling M, Kosek E, Ingvar M. 282 INCREASED SENSITIVITY TO PAIN FOLLOWING A SINGLE OPIATE DOSE IS INFLUENCED BY THE COMT val158met POLYMORPHISM. European Journal of Pain. 2009;13(S1)
Further evidence for the role of 5-HTTLPR and BDNFval66met in affect - Support for neuroimaging data from self reported stress sensitivity
No full textLonsdorf T, Golkar A, Schalling M, Öhman A. Further evidence for the role of 5-HTTLPR and BDNFval66met in affect - Support for neuroimaging data from self reported stress sensitivity. NeuroImage. 2009;47: S139
Temporal and spatial variability in speakers with Parkinson's Disease and Friedreich's Ataxia
No full textSpeech variability in groups of speakers with Parkinson's disease (PD) and with Friedreich's ataxia was compared with healthy controls. Speakers repeated the same phrase 20 times at one of two rates (fast or habitual). A non-linear analysis of variability was performed which used some of the principles behind the spatio-temporal index (STI). The STI usually employs variation in lip displacement over repetitions of the same utterance and a linear analysis of such signals is conducted to represent the combined variation in spatial and temporal control. When working with patients, audio measures (here we used speech energy) are preferred over kinematics ones as they are minimally disruptive to speech. Non-linear methods allow spatial variability to be estimated separately from temporal variability. The results are tentatively interpreted as showing that PD speakers were distinguished from healthy control speakers in spatial variability and ataxic speakers were distinguished from controls in temporal variability. These findings are consistent with the speech symptoms reported for these disorders. We conclude that the non-linear analysis using the speech energy measure is worth investigating further as it is potentially revealing of the differences underlying these two pathologies
Attention biases and habituation of attention biases are associated with 5-HTTLPR and COMTval158met
No full textLonsdorf T, Juth P, Rohde C, Schalling M, Öhman A. Attention biases and habituation of attention biases are associated with 5-HTTLPR and COMTval158met. Cognitive, Affective, & Behavioral Neuroscience. 2014;14(1):354-363
Amygdala-dependent fear conditioning in humans is modulated by the BDNFval66met polymorphism.
No full textLonsdorf T, Weike AI, Golkar A, Schalling M, Hamm AO, Öhman A. Amygdala-dependent fear conditioning in humans is modulated by the BDNFval66met polymorphism. Behavioral Neuroscience. 2010;124(1):9-15
Neurological disorders and celiac disease
No full textCeliac disease (CD) determines neurologic manifestations in 10% of all CD patients. We describe the most common clinical manifestations as cerebellar ataxia, gluten encephalopathy, multiple sclerosis, peripheral neuropathies, sensorineural hearing loss, epilepsy, headache, depression, cognitive deficiencies and other less described clinical conditions. Our aim is to perform, as more as possible, a review about the most recent update on the topics in international literature. It is important to consider clinical neurological manifestations in celiac patients and to research these conditions also in the follow-up because they may start also one year after the start of gluten free diet (GFD) as peripheral neuropathy. The association with autism is analysed and possible new association with non-celiac gluten sensitivity (NCGS) are considered
Muscleblind localizes to nuclear foci of aberrant RNA in myotonic dystrophy types 1 and 2
No full textThe phenotypes in myotonic dystrophy types 1 and 2 (DM1 and DM2) are similar, suggesting a shared pathophysiologic mechanism. DM1 is caused by expansion of a CTG repeat in the DMPK gene. Pathogenic effects of this mutation are likely to be mediated, at least in part, by the expanded CUG repeat in mutant mRNA. The mutant transcripts are retained in the nucleus in multiple discrete foci. We investigated the possibility that DM2 is also caused by expansion of a CTG repeat or related sequence. Analysis of DNA by repeat expansion detection methods, and RNA by ribonuclease protection, did not show an expanded CTG or CUG repeat in DM2. However, hybridization of muscle sections with fluorescence-labeled CAG-repeat oligonucleotides showed nuclear foci in DM2 similar to those seen in DM1. Nuclear foci were present in all patients with symptomatic DM1 (n = 9) or DM2 (n = 9) but not in any disease controls or healthy subjects (n = 23). The foci were not seen with CUG- or GUC-repeat probes. Foci in DM2 were distinguished from DM1 by lower stability of the probe-target duplex, suggesting that a sequence related to the DM1 CUG expansion accumulates in the DM2 nucleus. Muscleblind proteins, which interact with expanded CUG repeats in vitro, localized to the nuclear foci in both DM1 and DM2. These results support the idea that nuclear accumulation of mutant RNA is pathogenic in DM1, suggest that a similar disease process occurs in DM2, and point to a role for muscleblind in the pathogenesis of both disorders
Clinical and genetic outcome determinants of Internet- and group-based cognitive behavior therapy for social anxiety disorder
No full textHedman E, Andersson E, Ljotsson B, Andersson G, Andersson E, Schalling M, Lindefors N, Ruck C. Clinical and genetic outcome determinants of Internet- and group-based cognitive behavior therapy for social anxiety disorder (SAD). Objective: No study has investigated clinical or genetic predictors and moderators of Internet-based cognitive behavior therapy (ICBT) compared with cognitive behavioral group therapy for (CBGT) for SAD. Identification of predictors and moderators is essential to the clinician in deciding which treatment to recommend for whom. We aimed to identify clinical and genetic (5-HTTLPR, COMTval158met, and BDNFval66met) predictors and moderators of ICBT and CBGT. Method: We performed three types of analyses on data from a sample comprising participants (N = 126) who had undergone ICBT or CBGT in a randomized controlled trial. Outcomes were i) end state symptom severity, ii) SAD diagnosis, and iii) clinically significant improvement. Results: The most stable predictors of better treatment response were working full time, having children, less depressive symptoms, higher expectancy of treatment effectiveness, and adhering to treatment. None of the tested gene polymorphisms were associated with treatment outcome. Comorbid general anxiety and depression were moderators meaning that lower levels were associated with a better treatment response in ICBT but not in CBGT. Conclusion: We conclude that demographic factors, symptom burden, adherence, and expectations may play an important role as predictors of treatment outcome. The investigated gene polymorphisms do not appear to make a difference.</p
Possible Implications for Gene-Environment Interaction in Anxiety Disorder
No full textLonsdorf T, Weike AI, Nikamo P, Schalling M, Hamm AO, Öhman A. Genetic Gating of Human Fear Learning and Extinction. Psychological Science. 2009;20(2):198-206.Pavlovian fear conditioning is a widely used model of the acquisition and extinction of fear. Neural findings suggest that the amygdala is the core structure for fear acquisition, whereas prefrontal cortical areas are given pivotal roles in fear extinction. Forty-eight volunteers participated in a fear-conditioning experiment, which used fear potentiation of the startle reflex as the primary measure to investigate the effect of two genetic polymorphisms (5-HTTLPR and COMTval158met) on conditioning and extinction of fear. The 5-HTTLPR polymorphism, located in the serotonin transporter gene, is associated with amygdala reactivity and neuroticism, whereas the COMTval158met polymorphism, which is located in the gene coding for catechol-O-methyltransferase (COMT), a dopamine-degrading enzyme, affects prefrontal executive functions. Our results show that only carriers of the 5-HTTLPR s allele exhibited conditioned startle potentiation, whereas carriers of the COMT met/met genotype failed to extinguish conditioned fear. These results may have interesting implications for understanding gene-environment interactions in the development and treatment of anxiety disorders
Longitudinal evidence of the impact of normal thyroid stimulating hormone variations on cognitive functioning in very old age
No full textThe purpose of this study was to examine longitudinal associations among thyroid stimulating hormone (TSH) levels and cognitive performance. Data collected at the first three assessment times, approximately 3 years apart, are reported for the survivors (n=45) from a previously published cross-sectional study. Participants were aged 75–93 years at baseline, and data reported were collected in the Kungsholmen Project, a longitudinal project investigating aging and dementia. Analyses revealed that although declining verbal fluency and visuospatial abilities were accompanied by simultaneously declining TSH levels, the pattern of cross-sectional and longitudinal results are interpreted such that declining TSH levels may have caused episodic memory deficits later on. These results were obtained in the examination of 6-year but not 3-year change, and after removal of the cognitive variation associated with depressive mood symptoms
- …
