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Östermalm, Sweden

Mousavi-Nasab S.-M.-H.,Shahid Bahonar University of Kerman | Kormi-Nouri R.,Orebro University | Nilsson L.-G.,University of Stockholm | Nilsson L.-G.,Stockholm Brain Institute
British Journal of Psychology | Year: 2014

The present study examined the relationships between different types of social and cognitive activities and different types of episodic and semantic memory. A total of 794 adult men and women from five age cohorts (aged 65-85 at baseline), participating in the longitudinal Betula project on ageing, memory, and health, were included in the study. The participants were studied over 10 years (1995-2005) in three waves. Recognition and recall were used as episodic memory tasks, and knowledge and verbal fluency as semantic memory tasks. The results, after controlling for age, gender, education, and some diseases, including heart disease and hypertension, as covariates, showed unidirectional effects of social activity on episodic memory on all test occasions (β = .10). Also, episodic memory predicted change in cognitive activity for all test waves (β = .21-.22). Findings suggest that social activity can be seen as protective factor against memory decline. It also seems that episodic memory performance is a predictor of cognitive activity in old people. However, the opposite direction does not hold true. © 2013 The British Psychological Society.

Klaus A.,National Institute of Mental Health | Klaus A.,Karolinska Institutet | Klaus A.,Stockholm Brain Institute | Yu S.,National Institute of Mental Health | Plenz D.,National Institute of Mental Health
PLoS ONE | Year: 2011

The size distribution of neuronal avalanches in cortical networks has been reported to follow a power law distribution with exponent close to -1.5, which is a reflection of long-range spatial correlations in spontaneous neuronal activity. However, identifying power law scaling in empirical data can be difficult and sometimes controversial. In the present study, we tested the power law hypothesis for neuronal avalanches by using more stringent statistical analyses. In particular, we performed the following steps: (i) analysis of finite-size scaling to identify scale-free dynamics in neuronal avalanches, (ii) model parameter estimation to determine the specific exponent of the power law, and (iii) comparison of the power law to alternative model distributions. Consistent with critical state dynamics, avalanche size distributions exhibited robust scaling behavior in which the maximum avalanche size was limited only by the spatial extent of sampling ("finite size" effect). This scale-free dynamics suggests the power law as a model for the distribution of avalanche sizes. Using both the Kolmogorov-Smirnov statistic and a maximum likelihood approach, we found the slope to be close to -1.5, which is in line with previous reports. Finally, the power law model for neuronal avalanches was compared to the exponential and to various heavy-tail distributions based on the Kolmogorov-Smirnov distance and by using a log-likelihood ratio test. Both the power law distribution without and with exponential cut-off provided significantly better fits to the cluster size distributions in neuronal avalanches than the exponential, the lognormal and the gamma distribution. In summary, our findings strongly support the power law scaling in neuronal avalanches, providing further evidence for critical state dynamics in superficial layers of cortex.

Persson N.,University of Stockholm | Persson N.,Stockholm Brain Institute | Persson N.,Wayne State University | Ghisletta P.,University of Geneva | And 7 more authors.
NeuroImage | Year: 2014

We examined regional changes in brain volume in healthy adults (. N=. 167, age 19-79. years at baseline; N=. 90 at follow-up) over approximately two years. With latent change score models, we evaluated mean change and individual differences in rates of change in 10 anatomically-defined and manually-traced regions of interest (ROIs): lateral prefrontal cortex (LPFC), orbital frontal cortex (OF), prefrontal white matter (PFw), hippocampus (Hc), parahippocampal gyrus (PhG), caudate nucleus (Cd), putamen (Pt), insula (In), cerebellar hemispheres (CbH), and primary visual cortex (VC). Significant mean shrinkage was observed in the Hc, CbH, In, OF, and PhG, and individual differences in change were noted in all regions, except the OF. Pro-inflammatory genetic variants modified shrinkage in PhG and CbH. Carriers of two T alleles of interleukin-1β (. IL-1β C-511T, rs16944) and a T allele of methylenetetrahydrofolate reductase (. MTHFR C677T, rs1801133) polymorphisms showed increased PhG shrinkage. No effects of a pro-inflammatory polymorphism for C-reactive protein (. CRP-286C>A>T, rs3091244) or apolipoprotein (. APOE) ε4 allele were noted. These results replicate the pattern of brain shrinkage observed in previous studies, with a notable exception of the LPFC, thus casting doubt on the unique importance of prefrontal cortex in aging. Larger baseline volumes of CbH and In were associated with increased shrinkage, in conflict with the brain reserve hypothesis. Contrary to previous reports, we observed no significant linear effects of age and hypertension on regional brain shrinkage. Our findings warrant further investigation of the effects of neuroinflammation on structural brain change throughout the lifespan. © 2014 Elsevier Inc.

Savic I.,Stockholm Brain Institute | Arver S.,Karolinska Institutet
Cerebral Cortex | Year: 2014

Although it has been shown that cortical thickness (Cth) differs between sexes, the underlying mechanisms are unknown. Seeing as XXY males have 1 extra X chromosome, we investigated the possible effects of X- and sex-chromosome dosage on Cth by comparing data from 31 XXY males with 39 XY and 47 XX controls. Plasma testosterone and estrogen were also measured in an effort to differentiate between possible sex-hormone and sex-chromosome gene effects. Cth was calculated with FreeSurfer software. Parietal and occipital Cth was greater in XX females than XY males. In these regions Cth was inversely correlated with z-normalized testosterone. In the motor strip, the cortex was thinner in XY males compared with both XX females and XXY males, indicating the possibility of an X-chromosome gene-dosage effect. XXY males had thinner right superior temporal and left middle temporal cortex, and a thicker right orbitofrontal cortex and lingual cortex than both control groups. Based on these data and previous reports from women with XO monosomy, it is hypothesized that programming of the motor cortex is influenced by processes linked to X-escapee genes, which do not have Y-chromosome homologs, and that programming of the superior temporal cortex is mediated by X-chromosome escapee genes with Y-homologs. © The Author 2013. Published by Oxford University Press.

Petrovic P.,Stockholm Brain Institute | Kalso E.,University of Helsinki | Petersson K.M.,Stockholm Brain Institute | Petersson K.M.,FARO | And 3 more authors.
Pain | Year: 2010

Behavioral studies have suggested that placebo analgesia is partly mediated by the endogenous opioid system. Expanding on these results we have shown that the opioid-receptor-rich rostral anterior cingulate cortex (rACC) is activated in both placebo and opioid analgesia. However, there are also differences between the two treatments. While opioids have direct pharmacological effects, acting on the descending pain inhibitory system, placebo analgesia depends on neocortical top-down mechanisms. An important difference may be that expectations are met to a lesser extent in placebo treatment as compared with a specific treatment, yielding a larger error signal. As these processes previously have been shown to influence other types of perceptual experiences, we hypothesized that they also may drive placebo analgesia. Imaging studies suggest that lateral orbitofrontal cortex (lObfc) and ventrolateral prefrontal cortex (vlPFC) are involved in processing expectation and error signals. We re-analyzed two independent functional imaging experiments related to placebo analgesia and emotional placebo to probe for a differential processing in these regions during placebo treatment vs. opioid treatment and to test if this activity is associated with the placebo response. In the first dataset lObfc and vlPFC showed an enhanced activation in placebo analgesia vs. opioid analgesia. Furthermore, the rACC activity co-varied with the prefrontal regions in the placebo condition specifically. A similar correlation between rACC and vlPFC was reproduced in another dataset involving emotional placebo and correlated with the degree of the placebo effect. Our results thus support that placebo is different from specific treatment with a prefrontal top-down influence on rACC. © 2010 International Association for the Study of Pain.

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