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Lanfredi M.,Irccs Istituto Centro San Giovanni Of Dio Fatebenefratelli | Zoppei S.,University of Verona | Ferrari C.,Irccs Istituto Centro San Giovanni Of Dio Fatebenefratelli | Bonetto C.,University of Verona | And 54 more authors.
European Psychiatry

Introduction: Individual social capital has been recognized as having an important role for health and well-being. We tested the hypothesis that poor social capital increases internalized stigma and, in turn, can reduce empowerment among people with major depressive disorder (MDD). Materials and methods: This is a cross-sectional multisite study conducted on a sample of 516 people with MDD in 19 European countries. Structural Equation Models were developed to examine the direct and indirect effects of self-stigma and social capital on empowerment. Results: Social capital and self-stigma accounted for 56% of the variability in empowerment. Higher social capital was related to lower self-stigma (r=. -0.72, P<. 0.001) which, in turn, partially mediated the relationship between social capital and empowerment (r=. 0.38, P<. 0.001). Conclusions: Social capital plays a key role in the appraisal of empowerment, both directly and through the indirect effect mediated by self-stigma. In order to improve empowerment of people with MDD, we identify strategies to foster individual social capital, and to overcome the negative consequences related to self-stigma for attainment of life goals. © 2014 Elsevier Masson SAS. Source

Rohrer J.D.,University College London | Nicholas J.M.,University College London | Nicholas J.M.,London School of Hygiene and Tropical Medicine | Cash D.M.,University College London | And 62 more authors.
The Lancet Neurology

Background: Frontotemporal dementia is a highly heritable neurodegenerative disorder. In about a third of patients, the disease is caused by autosomal dominant genetic mutations usually in one of three genes: progranulin (. GRN), microtubule-associated protein tau (. MAPT), or chromosome 9 open reading frame 72 (. C9orf72). Findings from studies of other genetic dementias have shown neuroimaging and cognitive changes before symptoms onset, and we aimed to identify whether such changes could be shown in frontotemporal dementia. Methods: We recruited participants to this multicentre study who either were known carriers of a pathogenic mutation in GRN, MAPT, or C9orf72, or were at risk of carrying a mutation because a first-degree relative was a known symptomatic carrier. We calculated time to expected onset as the difference between age at assessment and mean age at onset within the family. Participants underwent a standardised clinical assessment and neuropsychological battery. We did MRI and generated cortical and subcortical volumes using a parcellation of the volumetric T1-weighted scan. We used linear mixed-effects models to examine whether the association of neuropsychology and imaging measures with time to expected onset of symptoms differed between mutation carriers and non-carriers. Findings: Between Jan 30, 2012, and Sept 15, 2013, we recruited participants from 11 research sites in the UK, Italy, the Netherlands, Sweden, and Canada. We analysed data from 220 participants: 118 mutation carriers (40 symptomatic and 78 asymptomatic) and 102 non-carriers. For neuropsychology measures, we noted the earliest significant differences between mutation carriers and non-carriers 5 years before expected onset, when differences were significant for all measures except for tests of immediate recall and verbal fluency. We noted the largest Z score differences between carriers and non-carriers 5 years before expected onset in tests of naming (Boston Naming Test -0·7; SE 0·3) and executive function (Trail Making Test Part B, Digit Span backwards, and Digit Symbol Task, all -0·5, SE 0·2). For imaging measures, we noted differences earliest for the insula (at 10 years before expected symptom onset, mean volume as a percentage of total intracranial volume was 0·80% in mutation carriers and 0·84% in non-carriers; difference -0·04, SE 0·02) followed by the temporal lobe (at 10 years before expected symptom onset, mean volume as a percentage of total intracranial volume 8·1% in mutation carriers and 8·3% in non-carriers; difference -0·2, SE 0·1). Interpretation: Structural imaging and cognitive changes can be identified 5-10 years before expected onset of symptoms in asymptomatic adults at risk of genetic frontotemporal dementia. These findings could help to define biomarkers that can stage presymptomatic disease and track disease progression, which will be important for future therapeutic trials. Funding: Centres of Excellence in Neurodegeneration. © 2015 Rohrer et al. Source

Rossi R.,Istituto Centro San Giovanni Of Dio Fatebenefratelli | Lanfredi M.,Istituto Centro San Giovanni Of Dio Fatebenefratelli | Pievani M.,Neuroimaging And Telemedicine Istituto Centro San Giovanni Of Dio Fatebenefratelli | Boccardi M.,Neuroimaging And Telemedicine Istituto Centro San Giovanni Of Dio Fatebenefratelli | And 6 more authors.
Psychiatry Research - Neuroimaging

Hippocampal abnormalities may be implicated in the pathophysiology of mental disorders with affective symptoms such as borderline personality disorder (BPD) and bipolar disorder (BD). We aimed to investigate hippocampal morphology in BPD and BD patients, compared to 1:1 age- and sex-matched healthy controls (HC) using a three-dimensional mapping method. Manual tracing of the hippocampi on magnetic resonance imaging (MRI) images was performed on 26 patients with BPD (age: 38 ± 11; sex (f): 16 (61%)) and 15 with BD (age: 44 ± 9; sex (f): 5 (33%)) and their age- and sex-matched HC (for BPD: n= 26; age: 38 ± 11; sex (f): 16 (61%); for BD: n= 15; age: 44 ± 9; sex (f): 5 (33%)). Compared to their reference groups, BPD patients showed smaller hippocampal volume bilaterally. The BD group showed significantly smaller right hippocampal volumes. In the surface maps, alterations were localized to different hippocampal sectors for the two groups: the CA1 regions and subiculum, bilaterally, in BPD, and the right dentate gyrus in the BD group. These differences persisted after controlling for alcohol and substance abuse. BPD and BD groups may exhibit distinct patterns of volumetric MRI changes in hippocampal subdivisions that might be related to the clinical phenomenology of each disorder. © 2012 Elsevier Ireland Ltd. Source

Rossi R.,Irccs Istituto Centro San Giovanni Of Dio Fatebenefratelli | Lanfredi M.,Irccs Istituto Centro San Giovanni Of Dio Fatebenefratelli | Pievani M.,Istituto Centro San Giovanni Of Dio Fatebenefratelli | Boccardi M.,Istituto Centro San Giovanni Of Dio Fatebenefratelli | And 17 more authors.
European Psychiatry

Background: Borderline personality disorder (BPD) is a chronic condition with a strong impact on patients' affective, cognitive and social functioning. Neuroimaging techniques offer invaluable tools to understand the biological substrate of the disease. We aimed to investigate gray matter alterations over the whole cortex in a group of Borderline Personality Disorder (BPD) patients compared to healthy controls (HC). Methods: Magnetic resonance-based cortical pattern matching was used to assess cortical gray matter density (GMD) in 26 BPD patients and in their age- and sex-matched HC (age: 38. ±. 11; females: 16, 61%). Results: BPD patients showed widespread lower cortical GMD compared to HC (4% difference) with peaks of lower density located in the dorsal frontal cortex, in the orbitofrontal cortex, the anterior and posterior cingulate, the right parietal lobe, the temporal lobe (medial temporal cortex and fusiform gyrus) and in the visual cortex ( P<. 0.005). Our BPD subjects displayed a symmetric distribution of anomalies in the dorsal aspect of the cortical mantle, but a wider involvement of the left hemisphere in the mesial aspect in terms of lower density. A few restricted regions of higher density were detected in the right hemisphere. All regions remained significant after correction for multiple comparisons via permutation testing. Conclusions: BPD patients feature specific morphology of the cerebral structures involved in cognitive and emotional processing and social cognition/mentalization, consistent with clinical and functional data. © 2014 Elsevier Masson SAS. Source

van der Zee J.,University of Antwerp | van der Zee J.,A+ Network | Bettens K.,University of Antwerp | Bettens K.,A+ Network | And 63 more authors.
Neurobiology of Aging

Meta-analysis of existing genome-wide association studies on Alzheimer's disease (AD) showed subgenome-wide association of an intronic variant in the sequestosome 1 (SQSTM1) gene with AD. We performed targeted resequencing of SQSTM1 in Flanders-Belgian AD patients selected to be enriched for a genetic background (n = 435) and geographically matched nonaffected individuals (n = 872) to investigate the role of both common and rare SQSTM1 variants. Results were extended to the European early-onset dementia cohorts (926 early-onset Alzheimer's disease [EOAD] patients and 1476 nonaffected individuals). Of the 61 detected exonic variants in SQSTM1, the majority were rare (n = 57). Rare variant (minor allele frequency <0.01) burden analysis did not reveal an increased frequency of rare variants in EOAD patients in any of the separate study populations nor when meta-analyzing all cohorts. Common variants p.D292= and p.R312= showed nominal association with AD (odds ratiop.D292== 1.11 [95% confidence interval= 1-1.22], p= 0.04), only when including the Flanders-Belgian cohort in the meta-analysis. We cannot exclude a role of SQSTM1 genetic variability in late-onset AD, but our data indicate that SQSTM1 does not play a major role in the etiology of EOAD. © 2015 The Authors. Source

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