Made in Italy as a collective belief.A model of investment in stereotypes

This paper interprets for the fist time the phenomenon of the made in Italy as a collective belief. First, a conceptual framework is proposed for analysing the formation and evolution of collective beliefs, by characterizing precisely the way individuals are expected to behave in this respect. Then, we argue that different paths may end up provoking the emergence of a collective belief, and maintain that the made in Italy can be though of as the case of a collective belief about the inventive and creative Italian way of producing a specific set of goods. Afterwards, we point to the investment in public rituals as the way to actively foster this collective belief, and then interpret such process as an economic problem of providing a public good. We highlight the main collective action implications of such analysis, by modelling individuals’ behaviour in different settings. The analysis is focused on those characteristics that make the made in Italy a special public good, such as joint private benefits, asymmetries between agents, accession costs, and transaction costs. Finally, policy and institutional implications are explored, in terms of redistribution, proactive subsidization, and contract design.collective beliefs, public rituals, impure public goods

Autism with epilepsy: A neurodevelopmental association

Introduction The association between Autism Spectrum Disorders (ASD) and epilepsy has been extensively documented and the estimated prevalence varies, depending upon the selected population and the clinical characteristics. Children with early-onset epilepsy and early brain damage have a higher risk of presenting ASD compared to those without epilepsy. Genetic abnormalities are likely implicated in the association of ASD and epilepsy, although these abnormalities are currently detectable in only a small percentage of patients. Copy number variants (CNVs) with a low rate of occurrence (so-called rare variants) have been found to be implicated in these conditions as well. Furthermore, some genetic and medical conditions are associated with ASD and epilepsy. Currently the co-occurrence of autism and epilepsy is conceptualized as the result of common abnormal neurodevelopmental pathways. Synaptic dysfunction is likely to be involved in both disorders, as observed in preclinical models. There is no specificity of seizure type to be expected in children and adolescents with ASD compared to other neurodevelopmental disorders or epileptic syndromes. Treatment options include developmentally-based early interventions for ASD and medications for epilepsy. The aim of this article is to provide a brief overview of current research on the association of autism with epilepsy, from molecular basis to clinical characteristics. Conclusion Common neurodevelopmental pathways are probably at play in the association of autism with epilepsy. Synaptic abnormalities and genetic variations have been shown to be implicated in this complex condition

Excitation/Inhibition Modulators in Autism Spectrum Disorder: Current Clinical Research

Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by social and communication abnormalities. Heterogeneity in the expression and severity of the core and associated symptoms poses difficulties in classification and the overall clinical approach. Synaptic abnormalities have been observed in preclinical ASD models. They are thought to play a major role in clinical functional abnormalities and might be modified by targeted interventions. An imbalance in excitatory to inhibitory neurotransmission (E/I imbalance), through altered glutamatergic and GABAergic neurotransmission, respectively, is thought to be implicated in the pathogenesis of ASD. Glutamatergic and GABAergic agents have been tested in clinical trials with encouraging results as to efficacy and tolerability. Further studies are needed to confirm the role of E/I modulators in the treatment of ASD and on the safety and efficacy of the current agents. Copyright © 2021 Canitano and Palumbi

Autism Spectrum Disorders and Schizophrenia Spectrum Disorders: Excitation/Inhibition Imbalance and Developmental Trajectories

Autism spectrum disorders (ASD) and schizophrenia spectrum disorders (SSD) share clinical and genetic components that have long been recognized. The two disorders co-occur more frequently than would be predicted by their respective prevalence, suggesting that a complex, multifactor association is involved. However, DSM-5 maintains the distinction between ASD, with core social and communication impairments, and SSD, including schizophrenia (SCZ), with hallucinations, delusions, and thought disorder as essential features. ASD and SSD have common biological underpinnings that may emerge early in development and unfold over time. One of the hypotheses supporting the similarities in the social and cognitive disturbances of ASD and SSD relates to abnormalities in the ratio of excitatory to inhibitory cortical activity (E/I imbalance). E/I imbalance in neurodevelopmental disorders could be the consequence of abnormalities in genes coding for glutamatergic and GABAergic receptors or synaptic proteins followed by system derangements. SSD and ASD have been characterized as polygenic disorders in which to the onset and progression of disease is triggered by interactions among multiple genes. Mammalian target of rapamycin signaling is under intense investigation as a convergent altered pathway in the two spectrum disorders. Current understanding of shared and divergent patterns between ASD and SSD from molecular to clinical aspects is still incomplete and may be implemented by the research domain criteria approach

Role of Genetics in the Etiology of Autistic Spectrum Disorder: Towards a Hierarchical Diagnostic Strategy

Progress in epidemiological, molecular and clinical genetics with the development of new techniques has improved knowledge on genetic syndromes associated with autism spectrum disorder (ASD). The objective of this article is to show the diversity of genetic disorders associated with ASD (based on an extensive review of single-gene disorders, copy number variants, and other chromosomal disorders), and consequently to propose a hierarchical diagnostic strategy with a stepwise evaluation, helping general practitioners/pediatricians and child psychiatrists to collaborate with geneticists and neuropediatricians, in order to search for genetic disorders associated with ASD. The first step is a clinical investigation involving: (i) a child psychiatric and psychological evaluation confirming autism diagnosis from different observational sources and assessing autism severity; (ii) a neuropediatric evaluation examining neurological symptoms and developmental milestones; and (iii) a genetic evaluation searching for dysmorphic features and malformations. The second step involves laboratory and if necessary neuroimaging and EEG studies oriented by clinical results based on clinical genetic and neuropediatric examinations. The identification of genetic disorders associated with ASD has practical implications for diagnostic strategies, early detection or prevention of co-morbidity, specific treatment and follow up, and genetic counselin

Alzheimer's Disease Promotion by Obesity: Induced Mechanisms—Molecular Links and Perspectives

The incidence of AD is increasing in parallel with the increase in life expectancy. At the same time the prevalence of metabolic syndrome and obesity is reaching epidemic proportions in western populations. Stress is one of the major inducers of visceral fat and obesity development, underlying accelerated aging processes. Adipose tissue is at present considered as an active endocrine organ, producing important mediators involved in metabolism regulation as well as in inflammatory mechanisms. Insulin and leptin resistance has been related to the dysregulation of energy balance and to the induction of a chronic inflammatory status which have been recognized as important cofactors in cognitive impairment and AD initiation and progression. The aim of this paper is to disclose the correlation between the onset and progression of AD and the stress-induced changes in lifestyle, leading to overnutrition and reduced physical activity, ending with metabolic syndrome and obesity. The involved molecular mechanisms will be briefly discussed, and advisable guide lines for the prevention of AD through lifestyle modifications will be proposed