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Sökning: WFRF:(Schalling Martin) > Stockholms universitet

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1.
  • Franzén, Erika, et al. (författare)
  • The EXPANd trial : effects of exercise and exploring neuroplastic changes in people with Parkinson's disease
  • 2019
  • Ingår i: BMC Neurology. - : Springer Science and Business Media LLC. - 1471-2377. ; 19:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Parkinson's disease (PD) affects many physiological systems essential for balance control. Recent studies suggest that intensive and cognitively demanding physical exercise programs are capable of inducing plastic brain changes in PD. We have developed a highly challenging balance training (the HiBalance) program that emphasizes critical aspects of balance control through progressively introducing more challenging exercises which incorporates dual-tasking. Earlier studies have shown it to be effective in improving balance, gait and dual-tasking. The study design has thereafter been adjusted to link intervention-induced behavioral changes to brain morphology and function. Specifically, in this randomized controlled trial, we will determine the effects of the HiBalance program on balance, gait and cognition and relate this to task-evoked functional MRI (fMRI), as well as brain-derived neurotrophic factor (BDNF) in participants with mild-moderate PD.Methods: One hundred participants with idiopathic PD, Hoehn & Yahr stage 2 or 3, >= 60 years of age, >= 21 on Montreal Cognitive Assessment will be recruited in successive waves and randomized into either the HiBalance program or to an active control group (the HiCommunication program, targeting speech and communication). Both interventions will be performed in small groups, twice a week with 1 h sessions for 10 weeks. In addition, a 1 h, once a week, home exercise program will also be performed. A double-blinded design will be used. At the pre- and post-assessments, participants will be assessed on balance (main outcome), gait, cognitive functions, physical activity, voice/speech function, BDNF in serum and fMRI (3 T Philips) during performance of motor-cognitive tasks.Discussion: Since there is currently no cure for PD, findings of neuroplastic brain changes in response to exercise would revolutionize the way we treat PD, and, in turn, provide new hope to patients for a life with better health, greater independence and improved quality of life.
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2.
  • Lindstedt, Fredrik, et al. (författare)
  • Serotonin-1A Receptor Polymorphism (rs6295) Associated with Thermal Pain Perception
  • 2012
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 7:8
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Serotonin (5-HT) is highly involved in pain regulation and serotonin-1A (5-HT1A) receptors are important in determining central 5-HT tone. Accordingly, variation in the 5-HT1A receptor gene (HTR1A) may contribute to inter-individual differences in human pain sensitivity. The minor G-allele of the HTR1A single nucleotide polymorphism (SNP) rs6295 attenuates firing of serotonergic neurons and reduces postsynaptic expression of the receptor. Experiments in rodents suggest that 5-HT1A-agonism modulates pain in opposite directions at mild compared to high noxious intensities. Based upon this and several other similar observations, we hypothesized that G-carriers would exhibit a relative hypoalgesia at mild thermal stimuli but tend towards hyperalgesia at higher noxious intensities. Methods: Fourty-nine healthy individuals were selectively genotyped for rs6295. Heat-and cold-pain thresholds were assessed along with VAS-ratings of a range of suprathreshold noxious heat intensities (45 degrees C-49 degrees C). Nociceptive-flexion reflex (NFR) thresholds were also assessed. Results: Volunteers did not deviate significantly from Hardy-Weinberg equilibrium. G-carriers were less sensitive to threshold-level thermal pain. This relative hypoalgesia was abolished at suprathreshold noxious intensities where G-carriers instead increased their ratings of heat-pain significantly more than C-homozygotes. No differences with regard to NFR-thresholds emerged. Conclusion/Significance: To the best of our knowledge this is the first study of human pain perception on the basis of variation in HTR1A. The results illustrate the importance of including a range of stimulus intensities in assessments of pain sensitivity. In speculation, we propose that an attenuated serotonergic tone may be related to a 'hypo- to hyperalgesic' response-pattern. The involved mechanisms could be of clinical interest as variation in pain regulation is known to influence the risk of developing pain pathologies. Further investigations are therefore warranted.
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3.
  • 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.
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4.
  • Freidle, M., et al. (författare)
  • Behavioural and neuroplastic effects of a double-blind randomised controlled balance exercise trial in people with Parkinson's disease
  • 2022
  • Ingår i: Npj Parkinsons Disease. - : Springer Science and Business Media LLC. - 2373-8057. ; 8:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Balance dysfunction is a disabling symptom in people with Parkinson's disease (PD). Evidence suggests that exercise can improve balance performance and induce neuroplastic effects. We hypothesised that a 10-week balance intervention (HiBalance) would improve balance, other motor and cognitive symptoms, and alter task-evoked brain activity in people with PD. We performed a double-blind randomised controlled trial (RCT) where 95 participants with PD were randomised to either HiBalance (n = 48) or a control group (n = 47). We found no significant group by time effect on balance performance (b = 0.4 95% CI [- 1, 1.9], p = 0.57) or on our secondary outcomes, including the measures of task-evoked brain activity. The findings of this well-powered, double-blind RCT contrast previous studies of the HiBalance programme but are congruent with other double-blind RCTs of physical exercise in PD. The divergent results raise important questions on how to optimise physical exercise interventions for people with PD.
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5.
  • Stenvinkel, Peter, et al. (författare)
  • Biomimetics provides lessons from nature for contemporary ways to improve human health
  • 2021
  • Ingår i: Journal of Clinical and Translational Science. - : Cambridge University Press (CUP). - 2059-8661. ; 5:1
  • Forskningsöversikt (refereegranskat)abstract
    • Homo sapiens is currently living in serious disharmony with the rest of the natural world. For our species to survive, and for our well-being, we must gather knowledge from multiple perspectives and actively engage in studies of planetary health. The enormous diversity of species, one of the most striking aspects of life on our planet, provides a source of solutions that have been developed through evolution by natural selection by animals living in extreme environments. The food system is central to finding solutions; our current global eating patterns have a negative impact on human health, driven climate change and loss of biodiversity. We propose that the use of solutions derived from nature, an approach termed biomimetics, could mitigate the effects of a changing climate on planetary health as well as human health. For example, activation of the transcription factor Nrf2 may play a role in protecting animals living in extreme environments, or animals exposed to heat stress, pollution and pesticides. In order to meet these challenges, we call for the creation of novel interdisciplinary planetary health research teams.
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