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Valentina Moschini

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2 papers

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YNICL Journal 2025 Journal Article

Beyond language: empathy and emotion recognition deficits in primary progressive aphasias

Giulia Giacomucci
Alice Pieri
Valentina Moschini
Chiara Crucitti
Sonia Padiglioni
Carmen Morinelli
Giulia Galdo
Filippo Emiliani

Although primary progressive aphasia (PPA) is considered a language disorder, increasing evidence points to the presence of social cognition impairments in PPA variants. The aims of this study were to explore empathy and emotion recognition deficits in the three PPA variants (sv-PPA, lv-PPA, nfv-PPA) and to identify their neural correlates. Eleven sv-PPA, 34 lv-PPA,11 nfv-PPA patients and 34 healthy controls (HC) were included in this study. Empathy was explored with the Interpersonal Reactivity Index (IRI) (Perspective Taking - PT, Fantasy - FT, Empathic Concern - EC, Personal Distress - PD), rated by caregivers before (T0) and after (T1) the onset of cognitive symptoms. Emotion recognition was evaluated with the Ekman 60Faces (EK-60F) Test and metabolic activity with [18F]FDG-PET. In all PPA variants, PT score was reduced from T0 to T1 (sv-PPA p = 0.014, lv-PPA p < 0.001, nfv-PPA p = 0.022) and PD score was increased (sv-PPA p = 0.033, lv-PPA p < 0.001, nfv-PPA p = 0.009). Only lv-PPA showed a decrease of FT score (p = 0.024), while EC was spared in all three variants. Sv-PPA patients had the worst performances in the EK-60F Test, followed by lv-PPA and, lastly, by nfv-PPA. Correlations between EK-60F scores and metabolic activity were found in sv-PPA and lv-PPA, highlighting the involvement of areas participating in the emotion recognition network: cingulate cortex, insula, temporal and orbitofrontal cortices and inferior frontal gyrus. All PPA variants exhibited impairments in cognitive empathy (PT) and heightened emotional contagion (PD). The most severe deficits in emotion recognition were shown by sv-PPA, while nfv-PPA was the less impaired variant.

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YNICL Journal 2023 Journal Article

Degradation of EEG microstates patterns in subjective cognitive decline and mild cognitive impairment: Early biomarkers along the Alzheimer’s Disease continuum?

Michael Lassi
Carlo Fabbiani
Salvatore Mazzeo
Rachele Burali
Alberto Arturo Vergani
Giulia Giacomucci
Valentina Moschini
Carmen Morinelli

Alzheimer's disease (AD) pathological changes may begin up to decades earlier than the appearance of the first symptoms of cognitive decline. Subjective cognitive decline (SCD) could be the first pre-clinical sign of possible AD, which might be followed by mild cognitive impairment (MCI), the initial stage of clinical cognitive decline. However, the neural correlates of these prodromic stages are not completely clear yet. Recent studies suggest that EEG analysis tools characterizing the cortical activity as a whole, such as microstates and cortical regions connectivity, might support a characterization of SCD and MCI conditions. Here we test this approach by performing a broad set of analyses to identify the prominent EEG markers differentiating SCD (n = 57), MCI (n = 46) and healthy control subjects (HC, n = 19). We found that the salient differences were in the temporal structure of the microstates patterns, with MCI being associated with less complex sequences due to the altered transition probability, frequency and duration of canonic microstate C. Spectral content of EEG, network connectivity, and spatial arrangement of microstates were instead largely similar in the three groups. Interestingly, comparing properties of EEG microstates in different cerebrospinal fluid (CSF) biomarkers profiles, we found that canonic microstate C displayed significant differences in topography in AD-like profile. These results show that the progression of dementia might be associated with a degradation of the cortical organization captured by microstates analysis, and that this leads to altered transitions between cortical states. Overall, our approach paves the way for the use of non-invasive EEG recordings in the identification of possible biomarkers of progression to AD from its prodromal states.

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