Lack of abstract thinking, known as , is a well-known psychopathological feature of schizophrenia, reflecting the tendency to adhere to concrete aspects of stimuli and figurative language comprehension difficulties. Inspired by the similarity between 'concretism' as defined in psychopathology and 'concreteness' as defined in linguistics, namely a semantic dimension linked to perceptual experience, we tested the novel hypothesis that impairment in deriving figurative meanings is related to impairment at the semantic level, involving concreteness. We analysed speech samples from 63 individuals with schizophrenia and 47 controls, who were asked to verbalise the meaning of idioms, metaphors, and proverbs.
View Article and Find Full Text PDFInvestigating amyloid-β (Aβ) peptides in solution is essential during the initial stages of developing lead compounds that can influence Aβ fibrillation while the peptide is still in a soluble state. The tendency of the Aβ(1-42) peptide to misfold in solution, correlated to the aetiology of Alzheimer's disease (AD), is one of the main hindrances to characterising its aggregation kinetics in a cell-mimetic environment. Moreover, the Aβ(1-42) aggregation triggers the unfolded protein response (UPR) in the endoplasmic reticulum (ER), leading to cellular dysfunction and multiple cell death modalities, exacerbated by reactive oxygen species (ROS), which damage cellular components and trigger inflammation.
View Article and Find Full Text PDFPrevious literature showed that people with schizophrenia have difficulties in humor comprehension and might differ from controls in the appreciation of humor, i.e., in perceived funniness.
View Article and Find Full Text PDFBackground: In the last decade, the kynurenine pathway (KP) has gained attention in the pathogenesis of cognitive impairment in schizophrenia being at the croassroad between neuroinflammation and glutamatergic and cholinergic neurotransmission. However, clinical findings are scarse and conflicting, and the specific contributions of these two systems to the neurobiology of cognitive symptoms are far from being elucidated. Furthermore, little is known about the molecular underpinnings of non-pharmacological interventions for cognitive improvement, including rehabilitation strategies.
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