Unravelling neural correlates of empathy deficits in Subjective Cognitive Decline, Mild Cognitive Impairment and Alzheimer's Disease.

Empathy is the ability to understand (cognitive empathy) and to feel (affective empathy) what others feel. The aim of the study was to assess empathy deficit and neuronal correlates in Subjective Cognitive Decline (SCD), Mild Cognitive Impairment (MCI) and Alzheimer's Disease (AD) dementia. Twenty-four SCD, 41 MCI and 46 CE patients were included. Informer-rated Interpersonal Reactivity Index was used to explore cognitive (Perspective Taking-PT, Fantasy-FT) and affective (Empathic Concern-EC, Personal Distress-PD) empathy, before (T0) and after (T1) cognitive symptoms' onset. Emotion recognition ability was tested through Ekman-60 Faces Test. Cerebral FDG-PET SPM analysis was used to explore neural correlates underlying empathy deficits. FT-T1 scores were lower in AD compared to SCD (13.0 ± 8.0 vs 19.1 ± 4,7 p = 0.008), PD-T1 score were higher in AD compared to MCI and to SCD (27.00 ± 10.00 vs 25.3 ± 5.9 vs 20.5 ± 5.6, p = 0.001). A positive correlation was found between PT-T1 and metabolic disfunction of right middle gyrus (MFG) in MCI and AD. In AD group, a positive correlation between PT-T1 and insula and superior temporal gyrus (STG) metabolism was detected. A negative correlation was found between PD-T1 and superior parietal lobule metabolism in MCI, and between PD-T1 and STG metabolism in AD. Impairment of cognitive empathy starts at MCI stage. Increase of PD starts from preclinical phases and seems to be to be dissociated from cognitive decline. Loss of PT is related to a progressive involvement starting from right MFG in prodromal stage, extending to insula and STG in dementia. Heightened emotional contagion is probably related to derangement of mirror neurons systems in parietal regions in prodromal stages, and to impairment of temporal emotion inhibition system in advanced phases. Further studies are needed to clarify if alterations in emotional contagion might be a predictive feature of a cognitive decline driven by AD.