Bellvitge University Hospital Bellvitge Biomedical Research Institute

Spain

Bellvitge University Hospital Bellvitge Biomedical Research Institute

Spain
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Ansoleaga B.,Bellvitge University Hospital Bellvitge Biomedical Research Institute | Jove M.,University of Lleida | Schluter A.,Lhospitalet Of Llobregat | Garcia-Esparcia P.,Bellvitge University Hospital Bellvitge Biomedical Research Institute | And 9 more authors.
Neurobiology of Aging | Year: 2015

The neuroprotective role of adenosine and the deregulation of adenosine receptors in Alzheimer's disease (AD) have been extensively studied in recent years. However, little is known about the involvement of purine metabolism in AD. We started by analyzing gene expression in the entorhinal cortex of human controls and AD cases with whole-transcript expression arrays. Once we identified deregulation of the cluster purine metabolism, messenger RNA expression levels of 23 purine metabolism genes were analyzed with qRT-PCR in the entorhinal cortex, frontal cortex area 8, and precuneus at stages I-II, III-IV, and V-VI of Braak and Braak and controls. APRT, DGUOK, POLR3B, ENTPD3, AK5, NME1, NME3, NME5, NME7, and ENTPD2 messenger RNAs were deregulated, with regional variations, in AD cases when compared with controls. In addition, liquid chromatography mass spectrometry based metabolomics in the entorhinal cortex identified altered levels of dGMP, glycine, xanthosine, inosine diphosphate, guanine, and deoxyguanosine, all implicated in this pathway. Our results indicate stage- and region-dependent deregulation of purine metabolism in AD. © 2015 Elsevier Inc.


Goldberg X.,Bellvitge University Hospital Bellvitge Biomedical Research Institute | Goldberg X.,CIBER ISCIII | Cardoner N.,Bellvitge University Hospital Bellvitge Biomedical Research Institute | Cardoner N.,CIBER ISCIII | And 26 more authors.
Journal of Obsessive-Compulsive and Related Disorders | Year: 2016

Background Individuals vary in their use of emotion regulation strategies and this variation has been associated with obsessive-compulsive disorder (OCD). Previous studies suggest that affect and cognitive rigidity mediate this association, but such mediation effects have not yet been tested in an integrated model of inter-individual variation of OC symptoms. Methods We used a total sample of 111 subjects (79 OCD patients and 32 controls) and a path-analytic approach to simultaneously explore the associations between two emotion regulation strategies (i.e. cognitive reappraisal and expressive suppression), positive and negative affect, and cognitive rigidity with obsessive-compulsive symptoms as the outcome variable. Results Results showed that 49% of the variance of OC symptoms was explained by the best-fitting model (χ2=0.915, p=0.922, df=4). Cognitive reappraisal was associated with reduced presence/severity of OC symptoms, and this association was mediated by positive affect and decreased cognitive rigidity. In contrast, expressive suppression was associated with negative affect, increased cognitive rigidity and increased presence/severity of OC symptoms. Conclusions A deep-rooted interconnection between emotion and cognition – indicated by both full and partial mediations – is a key mechanism underlying vulnerability to OC symptoms. © 2016 Elsevier Ltd


Petrov D.,University of Barcelona | Petrov D.,CIBER ISCIII | Pedros I.,Rovira i Virgili University | Pedros I.,CIBER ISCIII | And 18 more authors.
Biochimica et Biophysica Acta - Molecular Basis of Disease | Year: 2015

Global obesity is a pandemic status, estimated to affect over 2 billion people, that has resulted in an enormous strain on healthcare systems worldwide. The situation is compounded by the fact that apart from the direct costs associated with overweight pathology, obesity presents itself with a number of comorbidities, including an increased risk for the development of neurodegenerative disorders. Alzheimer disease (AD), the main cause of senile dementia, is no exception. Spectacular failure of the pharmaceutical industry to come up with effective AD treatment strategies is forcing the broader scientific community to rethink the underlying molecular mechanisms leading to cognitive decline. To this end, the emphasis is once again placed on the experimental animal models of the disease. In the current study, we have focused on the effects of a high-fat diet (HFD) on hippocampal-dependent memory in C57/Bl6 Wild-type (WT) and APPswe/PS1dE9 (APP/PS1) mice, a well-established mouse model of familial AD. Our results indicate that the continuous HFD administration starting at the time of weaning is sufficient to produce β-amyloid-independent, hippocampal-dependent memory deficits measured by a 2-object novel-object recognition test (NOR) in mice as early as 6. months of age. Furthermore, the resulting metabolic syndrome appears to have direct effects on brain insulin regulation and mitochondrial function. We have observed pathological changes related to both the proximal and distal insulin signaling pathway in the brains of HFD-fed WT and APP/PS1 mice. These changes are accompanied by a significantly reduced OXPHOS metabolism, suggesting that mitochondria play an important role in hippocampus-dependent memory formation and retention in both the HFD-treated and AD-like rodents at a relatively young age. © 2015 Elsevier B.V.


PubMed | Bellvitge University Hospital Bellvitge Biomedical Research Institute, Catalan Institution for Research and Advanced Studies, University of Lleida, University of Barcelona and Lhospitalet Of Llobregat
Type: Journal Article | Journal: Neurobiology of aging | Year: 2014

The neuroprotective role of adenosine and the deregulation of adenosine receptors in Alzheimers disease (AD) have been extensively studied in recent years. However, little is known about the involvement of purine metabolism in AD. We started by analyzing gene expression in the entorhinal cortex of human controls and AD cases with whole-transcript expression arrays. Once we identified deregulation of the cluster purine metabolism, messenger RNA expression levels of 23 purine metabolism genes were analyzed with qRT-PCR in the entorhinal cortex, frontal cortex area 8, and precuneus at stages I-II, III-IV, and V-VI of Braak and Braak and controls. APRT, DGUOK, POLR3B, ENTPD3, AK5, NME1, NME3, NME5, NME7, and ENTPD2 messenger RNAs were deregulated, with regional variations, in AD cases when compared with controls. In addition, liquid chromatography mass spectrometry based metabolomics in the entorhinal cortex identified altered levels of dGMP, glycine, xanthosine, inosine diphosphate, guanine, and deoxyguanosine, all implicated in this pathway. Our results indicate stage- and region-dependent deregulation of purine metabolism in AD.


PubMed | Rovira i Virgili University, Institute Investigacion Hospital 12 Of Octubre, University of Barcelona, Bellvitge University Hospital Bellvitge Biomedical Research Institute and 3 more.
Type: Journal Article | Journal: Biochimica et biophysica acta | Year: 2015

Global obesity is a pandemic status, estimated to affect over 2 billion people, that has resulted in an enormous strain on healthcare systems worldwide. The situation is compounded by the fact that apart from the direct costs associated with overweight pathology, obesity presents itself with a number of comorbidities, including an increased risk for the development of neurodegenerative disorders. Alzheimer disease (AD), the main cause of senile dementia, is no exception. Spectacular failure of the pharmaceutical industry to come up with effective AD treatment strategies is forcing the broader scientific community to rethink the underlying molecular mechanisms leading to cognitive decline. To this end, the emphasis is once again placed on the experimental animal models of the disease. In the current study, we have focused on the effects of a high-fat diet (HFD) on hippocampal-dependent memory in C57/Bl6 Wild-type (WT) and APPswe/PS1dE9 (APP/PS1) mice, a well-established mouse model of familial AD. Our results indicate that the continuous HFD administration starting at the time of weaning is sufficient to produce -amyloid-independent, hippocampal-dependent memory deficits measured by a 2-object novel-object recognition test (NOR) in mice as early as 6months of age. Furthermore, the resulting metabolic syndrome appears to have direct effects on brain insulin regulation and mitochondrial function. We have observed pathological changes related to both the proximal and distal insulin signaling pathway in the brains of HFD-fed WT and APP/PS1 mice. These changes are accompanied by a significantly reduced OXPHOS metabolism, suggesting that mitochondria play an important role in hippocampus-dependent memory formation and retention in both the HFD-treated and AD-like rodents at a relatively young age.

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