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Background: Bipolar Disorder (BD) is a severe chronic psychiatric disorder whose aetiology is still largely unknown. However, increasing literature reported the involvement of neurovascular factors in the pathophysiology of BD, suggesting that a measure of Cerebral Blood Flow (CBF) could be an important biomarker of the illness. Therefore, since, to date, Magnetic Resonance Perfusion Weighted Imaging (PWI) techniques, such as Dynamic Susceptibility Contrast (DSC) and Arterial Spin Labelling (ASL), are the most common approaches that allow non-invasive in-vivo perfusion measurements,this review aims to summarize the results from all PWI studies that evaluated the CBF in BD., Methods: A bibliographic search in PubMed up until May 2021 was performed. 16 PWI studies that used DSC or ASL sequences met our inclusion criteria., Results: Overall, the results supported the presence of hyper-perfusion in the cingulate cortex and fronto-temporal regions, as well as the presence of hypo-perfusion in the cerebellum in BD, compared with both healthy controls and patients with unipolar depression. CBF changes after cognitive and aerobic training, as well as in relation with other physiological, clinical, and neurocognitive variables were also reported., Limitations: The heterogeneity across the studies, in terms of experimental designs, sample selection, and methodological approach employed, limited the studies' comparison., Conclusions: These findings showed CBF alterations in the cingulate cortex, fronto-temporal regions, and cerebellum in BD, suggesting that CBF may be an important pathophysiological marker of BD that merits further investigation to clarify the extent of neurovascular alterations., Competing Interests: Declaration of competing interest The authors report no conflicts of interest., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Major Depressive Disorder (MDD) is a disabling illness affecting more than 5% of the elderly population. Higher female prevalence and sex-specific symptomatology have been observed, suggesting that biologically-determined dimensions might affect the disease onset and outcome. Rumination and executive dysfunction characterize adult-onset MDD, but sex differences in these domains and in the related brain mechanisms are still largely unexplored. The present pilot study aimed to explore any interactions between adult-onset MDD and sex on brain morphology and brain function during a Go/No-Go paradigm. We hypothesized to detect diagnosis by sex effects on brain regions involved in self-referential processes and cognitive control. Twenty-four subjects, 12 healthy (HC) (mean age 68.7 y, 7 females and 5 males) and 12 affected by adult-onset MDD (mean age 66.5 y, 5 females and 7 males), underwent clinical evaluations and a 3T magnetic resonance imaging (MRI) session. Diagnosis and diagnosis by sex effects were assessed on regional gray matter (GM) volumes and task-related functional MRI (fMRI) activations. The GM volume analyses showed diagnosis effects in left mid frontal cortex ( p < 0.01), and diagnosis by sex effects in orbitofrontal, olfactory, and calcarine regions ( p < 0.05). The Go/No-Go fMRI analyses showed MDD effects on fMRI activations in left precuneus and right lingual gyrus, and diagnosis by sex effects on fMRI activations in right parahippocampal gyrus and right calcarine cortex ( p < 0.001, ≥ 40 voxels). Our exploratory results suggest the presence of sex-specific brain correlates of adult-onset MDD-especially in regions involved in attention processing and in the brain default mode-potentially supporting cognitive and symptom differences between sexes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Piani, Maggioni, Delvecchio, Ferro, Gritti, Pozzoli, Fontana, Enrico, Cinnante, Triulzi, Stanley, Battaglioli and Brambilla.)

This paper investigates changes between, and inequalities within, birth-cohorts in Italy, surrounding homeownership. Italy is a homeownership and familialistic society, where in recent decades an increasing 'generational divide' in employment prospects has opened up, as a side-effect of a partial and targeted labour market deregulation. Drawing on the interplay of macro-level constraints with micro-level factors, we discuss patterns of inequality in attaining homeownership between cohorts, arising from greater instability of employment for young adults, and within cohorts, stemming from class-based patterns of intergenerational wealth transmission. Our analytical strategy combines a sequential cohort design with two levels of analysis that simultaneously consider young people around the normative age of housing independence and wealth transmission from their families triggered by their leaving the nest. Longitudinal analyses apply random-effects probit models and linear probability distributed fixed-effects to panel data from the Bank of Italy (SHIW 1989-2016). Results show a decrease in homeownership attainment across cohorts, which can be partially ascribed to employment disadvantages faced by younger cohorts. On top of this, class-specific patterns of intergenerational transmission are in place: lower classes rely on timely housing wealth transfers, whereas upper classes are prepared to provide their children with an extended stream of financial transfers., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Background: Major Depressive Disorder (MDD) is a severe psychiatric disorder whose pathological mechanisms are largely unknown. In the field of immuno-psychiatry, several evidences suggested a prominent role of inflammation in MDD not only in peripheral immune system but also in the brain. To date, brain inflammation is traceable in vivo with Positron Emission Tomography (PET), through the quantification of the expression of 18-kda Translocator Protein (TSPO) by active microglia. In this context, this review aimed to summarize the results of all in vivo PET imaging studies that evaluated microglia activation in MDD., Methods: A bibliographic search in PubMed up to June 2020 was performed. A total of 9 studies that used first and second generation TSPO radiotracers met our inclusion criteria., Results: Overall the results suggested the presence of TSPO upregulation in MDD, especially in anterior cingulate cortex, prefrontal cortex, hippocampal formation and insula. Notably, from a therapeutic point of view, results suggested that the symptoms amelioration, caused by both antidepressant medication and cognitive behavioural therapy, may be accompanied by reduced inflammatory status in the brain. Finally, a positive effect of the anti-inflammatory treatment with a cyclooxygenase inhibitor has also been observed., Limitations: The heterogeneity across the studies in experimental designs, sample selection and methods limited the studies comparison., Conclusions: These findings supported the presence of neuroinflammation in MDD, suggesting that microgliosis may be an important pathophysiological mechanism that merits further investigation as a potential target for novel treatment strategies., (Copyright © 2021. Published by Elsevier B.V.)

Computer-assisted cognitive remediation (CACR) is a computer-based rehabilitation treatment aimed at improving cognition and at developing strategies that can be applied to various functional areas. Different protocols are currently used with great variability over the intensity and duration of treatments. In this study, we evaluated the effects of a brief and intensive CACR training (i.e., 15 sessions for 3 weeks) on cognitive domains, as well as the durability of cognitive gains and their generalization to functional areas, 3 months after CACR training. Thirty-eight patients with schizophrenia were recruited and assessed for psychopathology, cognitive performance, and functioning before the rehabilitative intervention. Patients were reassessed for cognition after CACR rehabilitation. Moreover, a subsample of 13 patients was evaluated for cognition and functioning 3 months after CACR completion. Results show significant improvements in multiple cognitive domains after CACR. Furthermore, 3 months after CACR completion, significant improvements were also detected in executive functions and daily functioning. This study suggests that a brief and intense CACR training is effective on cognitive and functional domains and that it could be feasible and affordable for health care services, thus offering patients the best options for fulfilling recovery goals.

We analyzed soluble vascular adhesion molecules (sVCAM-1), reactive oxygen metabolites (ROMs) level, total antioxidant status (TAS) and telediastolic left ventricular volume (TLVV) in patients with myocardial infarction undergoing reperfusion therapy and treated with antioxidant vitamins (AT) or placebo (P) before and for 1 month after reperfusion. After reperfusion, sVCAM-1 serum concentration, reactive oxygen metabolites level, and TLVV were significantly higher in patients treated with placebo than in those treated with antioxidant vitamins, while TAS was significantly higher in patients treated with antioxidant supplementation. We observed that 48 hours after reperfusion sVCAM-1 (P) vs sVCAM-1 (AT) was 2.03+/-0.5 vs 1.63+/-0.7 microg/ml with p < 0.01; ROMs (P) vs ROMs (AT) were 335.60+/-35.80 vs 307.50+/-47.10 U.CARR with p < 0.05; TAS (P) vs TAS (AT) was 526.47+/-44.24 vs 737.65+/-51.15 micromol/l with p < 0.01; 1 week after reperfusion TLVV (P) vs TLVV (AT) was 125.12+/-29.80 vs 119.40+/-29.40 ml with p < 0.05; 1 month after reperfusion TLVV (P) vs TLVV (AV) was 132.00+/-33.50 vs 123.40+/-21.60 ml with p < 0.05. In the first period after infarction, vitamin treatment improves the antioxidant system and reduces oxidative stress, inflammatory process and left ventricular remodeling.

Platelet recruitment crucially depends on amplification systems provided by autocrine and paracrine factors such as adenosine diphosphate. In inflammatory states, consumption of coagulation proteins, such as antithrombin aggravates the procoagulant state. In this study, we report that platelets express syndecan-4, an antithrombin-binding cell surface heparan sulphate proteoglycan, whose ligation with antithrombin inhibits activated platelet-dependent superoxide anion release from neutrophils by the limitation of adenosine diphosphate and adenosine triphosphate secretion in activated platelets. Adenosine triphosphate-induced platelet aggregation is reduced after treatment of platelets with antithrombin, which is reversed by blockade of syndecan-4. We further observed that antithrombin limits CD40 ligand expression in adenosine diphosphate-activated platelets and inhibits the shedding of syndecan-4 from activated platelets. Syndecan-4 appears to be directly involved in regulating platelet aggregation as anti-syndecan-4 antibody augments platelet aggregation. We suggest that antithrombin might exert beneficial effects in disseminated intravascular coagulation by reducing platelet activation, observed as inhibited CD40 ligand expression, syndecan-4 shedding, and adenosine diphosphate- and adenosine triphosphate-release from activated platelets with subsequent inhibition of neutrophil respiratory burst. From these data it is concluded that syndecan-4 may play important roles in the regulation of inflammatory effects of platelets.

Neurological paraneoplastic syndromes are a rare group of disorders that occur in 1-2% of people with malignancy. They are usually caused by an immune response, triggered by and directed against a tumour, that cross-reacts with protein expressed by the peripheral or central nervous system. Any part of the nervous system can be affected and patients often develop severe and permanent disability. Diagnosis can be difficult as in two-thirds of patients the neurological problems appear up to 5 years before the tumour manifests. However, certain of these syndromes are often associated with specific serum autoantibodies that can be useful both in diagnosis of the neurological syndrome and in focusing the search for a particular tumour. Thus, these antibodies can allow earlier identification and treatment of cancer and, potentially, a reduction in morbidity and mortality. It was only in the 1980s that the first anti-neuronal autoantibodies were characterized and their associations with clinical syndromes and tumours defined. Further antibodies have been isolated over the past 20 years and novel pathogenic mechanisms for several syndromes have been recognized. For example, voltage-gate ion channels seem to be a common target for autoantibodies involved in peripheral nerve diseases such as the Lambert-Eaton myasthenic syndrome and neuromyotonia (Isaacs' syndrome). However, the place of most paraneoplastic antibodies in the pathogenesis of central syndromes is yet to be fully elucidated.

Antithrombin-III exerts antiinflammatory effects via ligation of heparan sulfate proteoglycans. Here we show in vitro that recombinant human antithrombin-III attenuates CD11b/CD18 expression of activated neutrophils and monocytes in whole blood ex vivo. As leukocyte integrin expression is triggered by extracorporeal circulation, this observation may be of relevance for pharmacological treatment during cardiopulmonary bypass.