La por i el fàstic, dues cares de la mateixa moneda

De fet, ambdues emocions estan presents en alguns trastorns psicològics. Per això, psiquiatres de l'UAB estudien les nostres respostes fisiològiques a estímuls negatius provocats. Aquesta observació podria determinar perquè certes persones són més propenses a sofrir certes psicopatologies.De hecho, ambas emociones están presentes en algunos trastornospsicológicos. Por ello, psiquiatras de la UAB estudian nuestrasrespuestas fisiológicas a estímulos negativos provocados. Estaobservación podría determinar por qué ciertas personas son máspropensas a sufrir ciertas psicopatologías

Understanding the contribution of neural and physiological signal variation to the low repeatability of emotion-induced BOLD responses

Previous studies have reported low repeatability of BOLD activation measures during emotion processing tasks. It is not clear, however, whether low repeatability is a result of changes in the underlying neural signal over time, or due to insufficient reliability of the acquired BOLD signal caused by noise contamination. The aim of this study was to investigate the influence of “cleaning” the BOLD signal, by correcting for physiological noise and for differences in BOLD responsiveness, on measures of repeatability. Fifteen healthy volunteers were scanned on two different occasions, performing an emotion provocation task with faces (neutral, 50% fearful, 100% fearful) followed by a breath-hold paradigm to provide a marker of BOLD responsiveness. Repeatability of signal distribution (spatial repeatability) and repeatability of signal amplitude within two regions of interest (amygdala and fusiform gyrus) were estimated by calculating the intraclass correlation coefficient (ICC). Significant repeatability of signal amplitude was only found within the right amygdala during the perception of 50% fearful faces, but disappeared when physiological noise correction was performed. Spatial repeatability was higher within the fusiform gyrus than within the amygdala, and better at the group level than at the participant level. Neither physiological noise correction, nor consideration of BOLD responsiveness, assessed through the breath-holding, increased repeatability. The findings lead to the conclusion that low repeatability of BOLD response amplitude to emotional faces is more likely to be explained by the lack of stability in the underlying neural signal than by physiological noise contamination. Furthermore, reported repeatability might be a result of repeatability of task-correlated physiological variation rather than neural activity. This means that the emotion paradigm used in this study might not be useful for studies that require the BOLD response to be a stable measure of emotional processing, for example in the context of biomarkers

The functional connectivity between the nucleus accumbens and the ventromedial prefrontal cortex as an endophenotype for bipolar disorder

Background Alterations in functional connectivity between the nucleus accumbens (NAcc) and frontal cortices have been previously associated with the presence of psychiatric syndromes, among them bipolar disorder. Whether these alterations are a consequence or a risk factor for mental disorders remains unresolved. Methods This study included 35 bipolar participants, 30 of their resilient siblings, and 23 healthy controls to probe functional connectivity at rest between NAcc and the rest of the brain in a cross-sectional design. BOLD time series at rest from NAcc were used as seed-region in a woxel-wise correlational analysis. The strength of the correlations found were compared across groups after Fisher’s Z transformation. Results Our results showed increased functional connectivity between NAcc and a ventromedial prefrontal cortex (vmPFC) - comprising mainly the subgenual anterior cingulate - in patients compared to controls. Participants at increased genetic risk but yet resilient – i.e. unaffected siblings - showed functional connectivity values midway between the former two groups. Conclusions Our results are indicative of the potential for the connectivity between NAcc and the vmPFC to represent an endophenotype for bipolar disorder

Medical and neurobehavioural phenotypes in male and female carriers of Xp22.31 duplications in the UK Biobank

Deletions spanning the STS (steroid sulfatase) gene at Xp22.31 are associated with X-linked ichthyosis, corneal opacities, testicular maldescent, cardiac arrhythmia, and higher rates of developmental and mood disorders/traits, possibly related to the smaller volume of some basal ganglia structures. The consequences of duplication of the same genomic region have not been systematically assessed in large or adult samples, although evidence from case reports/series has indicated high rates of developmental phenotypes. We compared multiple measures of physical and mental health, cognition and neuroanatomy in male (n = 414) and female (n = 938) carriers of 0.8–2.5 Mb duplications spanning STS, and non-carrier male (n = 192, 826) and female (n = 227, 235) controls from the UK Biobank (recruited aged 40–69 from the UK general population). Clinical and self-reported diagnoses indicated a higher prevalence of inguinal hernia and mania/bipolar disorder respectively in male duplication carriers, and a higher prevalence of gastro-oesophageal reflux disease and blistering/desquamating skin disorder respectively in female duplication carriers; duplication carriers also exhibited reductions in several depression-related measures, and greater happiness. Cognitive function and academic achievement did not differ between comparison groups. Neuroanatomical analysis suggested greater lateral ventricle and putamen volume in duplication carriers. In conclusion, Xp22.31 duplications appear largely benign, but could slightly increase the likelihood of specific phenotypes (although results were only nominally-significant). In contrast to deletions, duplications might protect against depressive symptoms, possibly via higher STS expression/activity (resulting in elevated endogenous free steroid levels), and through contributing towards an enlarged putamen volume. These results should enable better genetic counselling of individuals with Xp22.31 microduplications

Polygenic risk for Alzheimer's disease shapes hippocampal scene-selectivity

Preclinical models of Alzheimer’s disease (AD) suggest APOE modulates brain function in structures vulnerable to AD pathophysiology. However, genome-wide association studies now demonstrate that AD risk is shaped by a broader polygenic architecture, estimated via polygenic risk scoring (AD-PRS). Despite this breakthrough, the effect of AD-PRS on brain function in young individuals remains unknown. In a large sample (N = 608) of young, asymptomatic individuals, we measure the impact of both (i) APOE and (ii) AD-PRS on a vulnerable cortico-limbic scene-processing network heavily implicated in AD pathophysiology. Integrity of this network, which includes the hippocampus (HC), is fundamental for maintaining cognitive function during ageing. We show that AD-PRS, not APOE, selectively influences activity within the HC in response to scenes, while other perceptual nodes remained intact. This work highlights the impact of polygenic contributions to brain function beyond APOE, which could aid potential therapeutic/interventional strategies in the detection and prevention of AD

Cortical abnormalities in bipolar disorder: An MRI analysis of 6,503 individuals from the ENIGMA-Bipolar Disorder Working Group

Despite decades of research, the pathophysiology of bipolar disorder (BD) is still not well understood. Structural brain differences have been associated with BD, but results from neuroimaging studies have been inconsistent. To address this, we performed the largest study to date of cortical gray matter thickness and surface area measures from brain MRI scans of 6,503 individuals including 1,837 unrelated adults with BD and 2,582 unrelated healthy controls for group differences while also examining the effects of commonly prescribed medications, age of illness onset, history of psychosis, mood state, age and sex differences on cortical regions. In BD, cortical gray matter was thinner in frontal, temporal and parietal regions of both brain hemispheres. BD had the strongest effects on left pars opercularis (Cohen’s d = -0.293; P = 1.71x10-21), left fusiform gyrus (d = -0.288; P = 8.25x10-21), and left rostral middle frontal cortex (d = -0.276; P = 2.99x10-19). Longer duration of illness (after accounting for age at time of scanning) was associated with reduced cortical thickness in frontal, medial parietal, and occipital regions. We found that several commonly prescribed medications, including lithium, antiepileptic, and antipsychotic treatment showed significant associations with cortical thickness and surface area, even after accounting for patients who received multiple medications. Further, we did not detect cortical differences associated with a history of psychosis or mood state at the time of scanning. Our analysis revealed previously undetected associations and provides an extensive analysis of potential confounding variables in neuroimaging studies of BD

Multimodal brain imaging reveals structural differences in Alzheimer's disease polygenic risk carriers: A study in healthy young adults

Background Recent genome-wide association studies have identified genetic loci that jointly make a considerable contribution to risk of developing Alzheimer’s disease (AD). Because neuropathological features of AD can be present several decades before disease onset, we investigated whether effects of polygenic risk are detectable by neuroimaging in young adults. We hypothesized that higher polygenic risk scores (PRSs) for AD would be associated with reduced volume of the hippocampus and other limbic and paralimbic areas. We further hypothesized that AD PRSs would affect the microstructure of fiber tracts connecting the hippocampus with other brain areas. Methods We analyzed the association between AD PRSs and brain imaging parameters using T1-weighted structural (n = 272) and diffusion-weighted scans (n = 197). Results We found a significant association between AD PRSs and left hippocampal volume, with higher risk associated with lower left hippocampal volume (p = .001). This effect remained when the APOE gene was excluded (p = .031), suggesting that the relationship between hippocampal volume and AD is the result of multiple genetic factors and not exclusively variability in the APOE gene. The diffusion tensor imaging analysis revealed that fractional anisotropy of the right cingulum was inversely correlated with AD PRSs (p = .009). We thus show that polygenic effects of AD risk variants on brain structure can already be detected in young adults. Conclusions This finding paves the way for further investigation of the effects of AD risk variants and may become useful for efforts to combine genotypic and phenotypic data for risk prediction and to enrich future prevention trials of AD